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BACKGROUND/AIMS: While DNA methylation and gastric microbiome are each associated with gastric cancer (GC), their combined role in predicting GC remains unclear. This study investigated the potential of a combined DNA methylation and gastric microbiome signature to predict Helicobacter pylori-negative GC. METHODS: In this case-control study, we conducted quantitative methylation-specific polymerase chain reaction to measure the methylation levels of DKK3, SFRP1, EMX1, NKX6-1, MIR124-3, and TWIST1 in the gastric mucosa from 75 H. pylori-negative patients, including chronic gastritis (CG), intestinal metaplasia (IM), and GC. A combined analysis of DNA methylation and gastric microbiome, using 16S rRNA gene sequencing, was performed in 30 of 75 patients. RESULTS: The methylation levels of DKK3, SFRP1, EMX1, MIR124-3, and TWIST1 were significantly higher in patients with GC than in controls (all q

Helicobacter pylori (H. pylori)-induced inflammation increases the risk of developing various upper gastrointestinal conditions which may progress to gastric cancer (CA). Early prediction and detection of infection are crucial for reducing cancer-induced mortality rates. The present case-control study aimed to investigate the combination of serum and molecular markers and H. pylori-associated gastroduodenal conditions as risk factors for predicting CA development in dyspeptic patients. Consecutive gastric biopsies and blood samples were collected from 100 adult dyspeptic patients. Serum IgG antibody levels against H. pylori were determined, and receiver operating characteristic (ROC) analysis was performed. The expression of the virulence genes cagA and vacA was evaluated by polymerase chain reaction (PCR). A significant association was reported between the disease condition and the status of several risk factors, such as family history, serum IgG antibody concentration, and the virulence genes cagA and vacA. Among the 71 H. pylori-positive patients, 35.2% (25/71) had CA. Both cagA and vacA genes were found in 46 out of 71 (64.7%) patients, and 92% (23/25) of CA patients carried the cagA+vacA s1 gene. ROC analysis of the serum IgG concentrations revealed AUC values of 0.81 and 0.78 for differentiating patients with non-ulcer dyspepsia from those with ulceration/inflammation and CA, respectively. The concordance between the IgG-positive and PCR-positive patients was 84% (k value=0.41). Patients who had a family history of CA with an increased serum IgG concentration and the presence of H. pylori cagA-vacA s1 genotypes may be considered strong predictors of future development of gastric pathologies, including CA. [ABSTRACT FROM AUTHOR]

Background: Detection of gastric cancer (GC) at early stages is an effective strategy for decreasing mortality. This study aimed to construct a prediction nomogram based on a questionnaire to assess the risk of developing GC. Methods: Our study comprised a total of 4379 participants (2326 participants from outpatient at Fengqing People's Hospital were considered for model development and internal validation, and 2053 participants from outpatients at the endoscopy center at the Seventh Affiliated Hospital of Sun Yat-Sen University were considered for independent external validation) and gastric mucosa status was determined by endoscopy and biopsies. The eligible participants in development cohort from Fengqing people's Hospital were randomly separated into a training cohort (n=1629, 70.0%) and an internal validation cohort (n=697, 30.0%). The relevant features were selected by a least absolute shrinkage and selection operator (LASSO), and the ensuing features were evaluated through multivariable logistic regression analysis. Subsequently, the variables were selected to construct a prediction nomogram. The discriminative ability and predictive accuracy of the nomogram were evaluated by the C-index and calibration plot, respectively. Decision curve analysis (DCA) curves were used for the assessment of clinical benefit of the model. This model was developed to estimate the risk of developing neoplastic lesions according to the "transparent reporting of a multivariable prediction model for individual prognosis or diagnosis" (TRIPOD) statement. Results: Six variables, including age, sex, alcohol consumption, cigarette smoking, education level, and Hp infection status, were independent risk factors for the development of neoplastic lesions. Thus, these variables were incorporated into the final nomogram. The AUC of the nomogram were 0.701, 0.657 and 0.699 in the training, internal validation, and external validation cohorts, respectively. The calibration curve showed that the nomogram was in good agreement with the observed outcomes. Compared to treatment of all patients or none, our nomogram showed a notably higher clinical benefit. Conclusion: This nomogram proved to be a convenient, cost-effective tool to effectively predict an individual's risk of developing neoplastic lesions, and it can act as a prescreening tool before gastroscopy. [ABSTRACT FROM AUTHOR]

Background: Several surveys conducted at slaughter sites have highlighted that gastric lesions are a widespread issue in fattening pigs, mainly due to feeding regimes. Diets with small particle sizes and low fibre contents guarantee high digestibility and performance but generate more rapid stomach emptying with a negative effect on gastric mucosa integrity. Providing fattening pigs with fibrous materials (e.g., straw provided in racks) or coarse fibrous ingredients (e.g., coarse silages) reduced the presence of gastric ulcers. The present research compares a traditional corn-soy-based diet with an experimental diet where bran and a portion of corn meal was substituted with whole ear and whole plant corn silages at the maximum dosages permitted by new Protected Designation of Origin for Italian dry-cured ham (20 and 10% of DM, respectively). This study aimed to examine the impact of the inclusion of corn silages in the diet on the productive performance of heavy Italian pigs and their ability to mitigate gastric mucosa damage. Results: The growth performances were satisfactory (750–800 g/d) given the advanced interval of growth of animals (from 120 to 180 kg). However, the inclusion of corn silages tended to reduce the growth rate by 5–6% due to the reduction of organic matter digestibility, without compromising the slaughter traits or the back-fat fatty acid profile. The experimental diet substantially affected both stomach development and mucosal integrity. The first consequence was an increase in stomach weight of approximately 6% (P < 0.01) but the most notable advantage of coarse feeding was a reduction in stomach damage severity, with a low number of cases with higher scores in animals fed coarse materials (P < 0.01). Conclusions: The dietary inclusion of corn silages (30% of diet DM) decrease effectivelly the severity of stomach damage in finishing heavy pigs. Based on the feeding trial performances, the perspective of feeding heavy pigs corn silage should consider specific agronomic and harvesting techniques to improve digestibility and not reduce the growth rate. [ABSTRACT FROM AUTHOR]

Simple Summary: Gastric polyps (GPs) are frequent gastric lesions, usually diagnosed incidentally. As upper gastrointestinal endoscopy becomes more frequent, the prevalence of GPs increases, with implications in clinical practice, as some of them can present different grades of malignant risk. The more common polyps are the epithelial ones, with a predominance of fundic gland polyps (FGPs) and gastric hyperplastic polyps (GHPs), in which prevalence varies according to local epidemiology. Up to now, the general recommendation is that all GPs should have histological evaluation by biopsy. However, novel advances in endoscopic techniques could allow for a more expectant management based on histopathological prediction by optical diagnosis. Further research and refinement of these techniques are necessary before their application in the clinical management of GPs. Gastric polyps (GPs) are common luminal lesions of the gastrointestinal tract, frequently detected incidentally in 1–6% of all upper gastrointestinal endoscopy. With the increasing use of endoscopy, the diagnosis of GPs has risen, highlighting the need for a thorough understanding of their pathophysiology and associated cancer risks. This review focuses on epithelial GPs, particularly fundic gland polyps (FGPs), hyperplastic polyps (GHPs) and gastric adenomas (GAs), discussing their classification, epidemiology, histopathology, endoscopic diagnosis, and current management. FGPs are predominantly associated with proton pump inhibitor (PPI) use and are common in regions with low Helicobacter pylori (Hp) prevalence, whereas GHPs are linked with Hp infection and chronic gastritis. GAs, although less common, have a significant risk of malignant transformation, especially in larger lesions. Management strategies vary according to polyp type, size, and dysplastic features, with resection recommended for high-risk lesions. Advances in endoscopic techniques, particularly narrow-band imaging (NBI), offer promising tools for differentiating between polyp types, potentially reducing the need for routine biopsies in the low-risk GPs. This review underscores the role of advanced imaging endoscopic techniques for the accurate classification and individualized management of GPs to mitigate the risk of gastric cancer. [ABSTRACT FROM AUTHOR]

Helicobacter pylori (H. pylori) infection is widely acknowledged as the primary risk factor for gastric cancer, facilitating its progression via the Correa cascade. Concurrently, Hexokinase Domain Containing 1 (HKDC1) has been implicated in the mediation of aerobic glycolysis, contributing to tumorigenesis across various cancers. However, the precise role of HKDC1 in the inflammatory transformation associated with H. pylori-induced gastric cancer remains elusive. In this study, transcriptome sequencing revealed a significant correlation between HKDC1 and H. pylori-induced gastric cancer. Subsequent validation using qRT-PCR, immunohistochemistry, and Western blot analysis confirmed elevated HKDC1 expression in both human and murine gastritis and gastric tumors. Moreover, in vitro and in vivo experiments demonstrated that H. pylori infection up-regulates TGF-β1 and p-Smad2, thereby activating the epithelial-mesenchymal transition (EMT) pathway, with HKDC1 playing a pivotal role. Suppression of HKDC1 expression or pharmacological inhibition of TGF-β1 reversed EMT activation, consequently reducing gastric cancer cell proliferation and metastasis. These results underscore HKDC1's essential contribution to H. pylori-induced gastric cancer progression via EMT activation. [ABSTRACT FROM AUTHOR]

Background: Chronic infection by Helicobacter pylori strains expressing cytotoxin-associated gene A (CagA) are the strongest risk factor for gastric cancer. CagA can be classified into East Asian-type and Western-type (CagAE and CagAW), with CagAE being more closely associated with gastric cancer. This study aimed to investigate the impact of CagAE on intracellular signaling pathways to explain its high oncogenicity. Results: Mutant H. pylori strains expressing either CagAE or CagAW were generated by transforming CagAE/W-expression plasmid into CagA-deleted G27 strain (G27ΔCagA). In human gastric epithelial cells (GES-1) infection, CagAE induced more severe cytopathic changes, including higher interleukin-8 (IL-8) secretion, reduced cell viability, more pronounced "hummingbird phenotype" alterations, and increased cell migration and invasion compared to CagAW. Transcriptome analysis revealed that CagAE had a stronger effect on the up-regulation of key intracellular processes, including tumor necrosis factor-ɑ (TNF-ɑ) signal pathway via nuclear factor kappa-B (NF-κB), inflammatory response, interferon-γ (IFN-γ) response, hypoxia, ultraviolet (UV) response, and Kirsten Rat Sarcoma Viral Oncogene Homolog (KRAS) signaling. A significant upregulation of hypoxia-related genes was a notable feature of CagAE. GES-1 cells infected with CagAE exhibited more severe intracellular hypoxia and higher levels of reactive oxygen species (ROS) than those infected with CagAW. Inhibition of hypoxia-inducible factor-1α (HIF-1α), which blocks hypoxia signaling, mitigated CagAE-induced cell migration, emphasizing the role of hypoxia in mediating CagAE effects. Conclusions: The study provides transcriptome evidence of CagA-associated intracellular regulation during H. pylori infection, demonstrating that CagAE exerts stronger effects on intracellular signaling than CagAW. These findings offer insights into the heightened carcinogenic potential of CagAE in H. pylori-induced gastric cancer. [ABSTRACT FROM AUTHOR]

Copyright of Baghdad Science Journal is the property of Republic of Iraq Ministry of Higher Education & Scientific Research (MOHESR) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Eupatilin, a flavone isolated from Artemisia species, exerts anti-inflammatory, anti-oxidative, and anti-neoplastic activities. However, the effects of eupatilin on H. pylori-associated gastritis remain unclear. Thus, this study aimed to investigate the anti-inflammatory effects of eupatilin on gastric epithelial cells infected with cytotoxin-associated gene A (CagA)-positive Helicobacter pylori. Materials and methods: AGS human gastric carcinoma cells were infected with a CagA-positive H. pylori strain and then treated with 10, 50, or 100 ng of eupatilin. After 24 h, the expression levels of CagA, phosphoinositide 3-kinase 1 (PI3K), nuclear factor (NF)-κB, interleukin (IL)-1β, and tumor necrosis factor (TNF)-α in the cell lysates were measured using western blotting, and the mRNA levels of IL-6, IL-8, and monocyte chemoattractant protein (MCP)-1 were measured using real-time polymerase chain reaction. Results: CagA translocation into AGS cells resulted in an elongated cell morphology, which was significantly suppressed by eupatilin treatment in a dose-dependent manner. Immunofluorescence staining for anti-CagA showed that eupatilin treatment dose-dependently inhibited CagA expression in the H. pylori-infected AGS cells. H. pylori infection increased the levels of pro-inflammatory cytokines including IL-1β, TNF-α, IL-6, IL-8, and MCP-1, and eupatilin treatment significantly reduced the levels of these cytokines in a dose-dependent manner. Additionally, eupatilin treatment dose-dependently suppressed the expression of PI3K and NF-κB. Conclusions: Eupatilin treatment demonstrated anti-inflammatory effects on CagA-positive H. pylori-infected gastric epithelial cells by inhibiting CagA translocation, thereby suppressing the NF-κB signaling pathway. These results suggest that eupatilin plays a protective role against CagA-positive H. pylori-induced gastritis. [ABSTRACT FROM AUTHOR]

Background: This study investigated clinicopathological factors associated with the visibility of early gastric cancer and the efficacy of linked color imaging. Methods: Patients with early gastric cancer who underwent endoscopic treatment between April 2021 and July 2022 were enrolled. All cases underwent white light imaging and linked color imaging. Three experts evaluated lesion visibility using a visual analog scale. A mean score ≥3 on white light imaging was defined as "good visibility", and <3 as "poor visibility". We extracted patient information and endoscopic and pathological data for the lesion and background mucosa, analyzed factors associated with the visibility of early gastric cancer, and compared visibility between white light imaging and linked color imaging. Results: Ninety-seven lesions were analyzed, with good visibility in 49 and poor visibility in 48. Multivariate analysis revealed small lesion size (odds ratio 1.89) and presence of endoscopic intestinal metaplasia (odds ratio 0.49) as significantly associated with the poor visibility of early gastric cancer. Mean visibility score was significantly higher for linked color imaging (P<0.001). Mean score for linked color imaging was significantly higher in the poor visibility group (P<0.001), but not significantly different in the good visibility group (P = 0.292). Mean score was significantly higher with linked color imaging in cases with endoscopic intestinal metaplasia (P = 0.0496) and lesions <20 mm in diameter (<10 mm, P = 0.002; 10–20 mm, P = 0.004). Conclusions: Lesion size and endoscopic intestinal metaplasia are associated with the visibility of early gastric cancer in white light imaging. Linked color imaging improves visibility of gastric cancer with these factors. [ABSTRACT FROM AUTHOR]

Key Clinical Message: Vigilant intraoperative inspection is crucial during gallbladder surgery to detect any abnormal tissue including the rare pyloric gland adenomas, which can be easily missed. Thorough examination and removal of unusual lymph nodes or thickened tissues are essential to prevent the risk of malignant transformation and ensure comprehensive patient care. Pyloric gland adenomas are uncommon tumors that can be discovered in various organs such as the stomach, gallbladder, and pancreas. Typically lacking noticeable symptoms, these tumors are categorized into subtypes, with the pyloric variant being the most frequent. The term "intracholecystic papillary‐tubular neoplasms (ICPN)" is used to emphasize growth patterns and associated risks. In a discussed case, a detached pyloric gland adenoma was identified incidentally during a cholecystectomy procedure. A 58‐year‐old obese male presented with upper abdominal pain, nausea, and vomiting. He was diagnosed with early cholecystitis caused by gallstones. Subsequently, during a laparoscopic cholecystectomy, a detached adenoma was discovered. Vigilant screening is crucial, as the identification of gallbladder pyloric gland adenomas is a rare occurrence that might be missed during gallbladder surgery. Any unusual lymph nodes or thickened tissues found in association with the gallbladder ought to be carefully removed, as they could potentially indicate detached gallbladder adenomas with a significant risk of becoming malignant. Failing to consider this possibility may subject the patient to prolonged risks if not meticulously examined. [ABSTRACT FROM AUTHOR]

Background: Limited information is available on gastric diseases in neonatal foals as compared with extensive studies in young, adult, and geriatric horses. Reports on fetuses are scarce. Objectives: Assess at necropsy stomachs of horse, donkey and mule fetuses in the third trimester of gestation to characterize lesions present during intrauterine life. Animals: Forty‐six fetal stomachs from both sexes (21 horses, 21 donkeys, and 4 mules) in the third trimester of gestation were collected from a processing plant immediately after slaughter. Methods: Measurements of longitudinal and transverse axes, weight and volume and gastric fluid pH were taken, and glandular and squamous mucosae were inspected. All findings of the gastric mucosa and measurements of the stomachs were presented descriptively. Groups were compared statistically, with significance level set at P <.05 for all evaluations. Results: All gastric contents had pH >5.8, and mules had larger stomachs and higher weights compared with horses (P <.05). Macroscopic lesions were classified as hyperemic, punctate, and erosive. Histopathologically, lesions were consistent with a chronic inflammatory process. Conclusions and Clinical Importance: Our study provides evidence of macroscopic and histopathological lesions in the gastric mucosae of equid fetuses in the last trimester of gestation. Relevant information for perinatology and neonatology is provided regarding the prevalence and classification of preulcerous lesions in equids before birth. [ABSTRACT FROM AUTHOR]

Gastric and duodenal ulcers are increasingly becoming global health burdens. The side effects of conventional treatments such as non-steroid anti-inflammatory drugs (NSAIDs), proton pump inhibitors (PPIs), antibiotics, and cytoprotective agents have necessitated the search for new medications. Plants are a rich source of active metabolites and herbal medicines have been used in the treatment of ulcers and cancers. In this study, we used in silico methods like molecular docking and MM-GBSA calculations to evaluate the effects of some anti-ulcer and anti-inflammatory phytochemicals on some key enzymes, cyclooxygenase (COX), and lipoxygenase (LOX), which are implicated in the protection and destruction of the gastric mucosa. The phytochemicals were retrieved from the literature and docked toward the binding sites of the three enzymes (COX-1, COX-2, and 5-LOX). Five compounds, rhamnetin, kaempferol, rutin, rosmarinic acid, and chlorogenic acid were observed to putatively bind to cyclooxygenase 2 (COX-2) and 5-lipoxygenase (5-LOX) but not to cyclooxygenase 1 (COX-1). The interaction mechanisms between these phytochemicals and the target proteins are discussed. The compounds' drug metabolism, pharmacokinetics, and toxicity have been evaluated to assess their suitability as potential next-generation anti-ulcer and anti-inflammatory drugs. [ABSTRACT FROM AUTHOR]

Objective(s): Some species of Prunus L. are popularly used to treat gastric ulcers. However, the possible healing mechanisms of the anti-ulcer activity of P. spinosa, which has proven antioxidant, anti-inflammatory, and wound-healing properties, are unclear. Materials and Methods: Ethanol extracts of P. spinosa fruits were administered orally at 100 mg/ kg and 200 mg/kg to Wistar albino rats, with an indomethacin-induced gastric ulcer model. The ulcerous areas on the stomach surface were examined macroscopically. Tissues were examined histopathologically and biochemically. LC-HRMS revealed the phytochemical content. Results: TNF-α, IL-6, IL-1β, IL-8, and NF-kB levels were higher in the gastric ulcer group than in the extract groups. The VEGF values did not differ in each group. A significant difference was found between the lansoprazole group and the high-dose P. spinosa group regarding PGE2 levels. A histopathologically significant difference was observed between the healthy group and the indomethacin-applied groups in terms of neutrophilic infiltration of the gastric mucosa. Ascorbic acid (1547.521 µg/g), homoprotocatechuic acid (1268.217 µg/g), and genistein (1014.462 µg/g) were found as the main compounds in the P. spinosa extract by LC-HRMS. Conclusion: Our results demonstrated that P. spinosa protected the gastric mucosa from inflammation and also modulated the PGE2 pathway. When considered in terms of TNF-α, IL-1 β, IL-8, IL-6, PGE2, and NF-kB values, it can be concluded that it has a similar or even more positive effect than the reference substance. P. spinosa showed its effects in a dose-dependent manner. [ABSTRACT FROM AUTHOR]

Background: In familial adenomatous polyposis (FAP) patients, fundic gland polyps (FGPs) have been considered a risk factor for gastric neoplasms. We speculated that FGPs in FAP patients spread directionally from the greater to the lesser curvature of the gastric body and investigated the relationship between the distribution of FGPs and gastric neoplasm development. Methods: We extracted 195 FAP patients from two institutions and reviewed their medical records. Gastric polyposis was classified based on the FGP distribution (P0, no FGPs; P1, localized in the fundus or greater curvature of the gastric body; P2, spreading to the anterior or posterior wall; P3, involving the proximal half of the lesser curvature; and P4, spreading from P3 to the anal side of the lesser curvature). Results: The 195 eligible patients were divided into the neoplasm group (n = 54, 28%) and the non-neoplasm group (n = 141, 72%). Overall, 24% of the patients were Helicobacter pylori (H. pylori)-positive. In the FGP distribution, the rate of patients with gastric neoplasm tended to increase significantly with each step towards an increasingly wide distribution from P0 to P4 in H. pylori-negative patients, but not in H. pylori-positive ones. In addition, in H. pylori-negative patients, the likelihood of neoplasm increased consistently from P0 to P4, with the highest odds ratio (95% confidence interval) at P4 of 14.1 (2.5–154.4). Furthermore, multivariate analysis showed P4 and Spigelman stage ≥III were significantly associated with gastric neoplasm development. Conclusion: FGP distribution was correlated with gastric neoplasm development in FAP patients. [ABSTRACT FROM AUTHOR]

Grapes, recognized as a nutritionally rich fruit, have been found through extensive research to contain various bioactive components. However, the roles of polysaccharides and their bioactive properties remain unclear. Based on this, in our research, four different grape polysaccharides were obtained using an enzymatic-assisted extraction method. We investigated and compared their physicochemical properties, antioxidant activities, and protective effects on gastric mucosa in mice. The results indicated that the monosaccharide compositions of these specific grape polysaccharides were similar; however, their molar ratios, molecular weights, and morphological characteristics varied. The results of radical scavenging tests revealed that red-fleshed grape polysaccharide (RFP) exhibited superior antioxidant properties. In vivo assessments demonstrated that RFP protects against gastric mucosal injury in mice by inhibiting inflammation and radical generation. Therefore, the polysaccharide from red-fleshed grape holds potential application value in the pharmaceutical and food industries. [ABSTRACT FROM AUTHOR]

Copyright of Microbes & Infectious Diseases is the property of Microbes & Infectious Diseases and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Tumor microenvironment (TME) immune cells and gastric mucosal microbiome constitute two vital elements of tumor tissue. Increasing evidence has elucidated their clinicopathological significance in predicting outcomes and therapeutic efficacy. However, comprehensive characterization of immune cell-associated microbiome signatures in the TME is still in the early stages of development. Here, we characterized the gastric mucosa microbiome and its associations with immune-activated related transcripts (IATs) in 170 GC tumor tissues and matched non-tumor tissues using 16s rRNA gene sequencing and quantitative reverse transcription-PCR. Microbial diversity and richness were significantly higher in GC tumor tissues than in non-tumor tissues. Differences in microbial composition between the groups were evident, with Firmicutes, Proteobacteria, Bacteroidota, Campilobacterota, Actinobacteria, Fusobacteriota, Verrucomicrobiota, Acidobacteriota, and Cyanobacteria being the dominant phyla in the gastric mucosal microbiota. Microbial interaction network analysis revealed distinctive centralities of oral bacteria (such as Fusobacterium, Porphyromonas, Prevotella, etc.) in both tumor and normal mucosae networks, suggesting their significant influence on GC microbial ecology. Furthermore, we analyzed the expression of IATs (CXCL9, CXCL10, GZMA, GZMB, PRF1, CD8A, IFNG, TBX2, and TNF) and characterized IAT-relevant gastric microbiome signatures in GC patients. Our results showed that the expression of CXCL9, CXCL10, GZMA, GZMB, PRF1 and IFNG was significantly higher in tumor tissues than in adjacent normal tissues in GC patients. Notably, high expression of IATs in tumor tissues was associated with improved survival in GC patients and could serve as a powerful predictor for disease-free survival. Additionally, analysis of IAT levels and mucosal microbiota diversity revealed a correlation between higher IAT expression and increased microbiota richness and evenness in the IATs high group, suggesting potential interactions between mucosal microbiota and tumor immunopathology. Spearman correlation analysis showed positive associations between IAT expression and specific mucosal bacterial species. Notably, Akkermansia muciniphila demonstrated potential involvement in modulating GZMB expression in the GC mucosal microenvironment. These findings underscore the importance of mucosal microbiota alterations in GC and suggest potential therapeutic targets focusing on modulating the tumor microbiota for improved clinical outcomes. The detailed characterization of these elements has profound implications for both treatment and survival prediction in GC. We observed that microbial diversity and richness were significantly higher in GC tumor tissues compared to non-tumor tissues. These differences highlight the unique microbial landscape of GC tumors and suggest that the microbiome could influence tumor development and progression. Importantly, our study demonstrated that high expression levels of IATs in GC tumor tissues were associated with improved patient survival. This suggests that IATs not only reflect immune activation but also serve as valuable biomarkers for predicting disease-free survival. The potential of IATs as predictive markers underscores their utility in guiding therapeutic strategies and personalizing treatment approaches. Moreover, the correlation between higher IAT expression and increased microbiota richness and evenness suggests that a diverse and balanced microbiome may enhance immune responses and contribute to better clinical outcomes. These findings highlight the critical need to consider mucosal microbiota alterations in GC management. Targeting the tumor microbiota could emerge as a promising therapeutic strategy, potentially leading to more effective treatments and improved patient outcomes. Understanding and modulating the microbiome’s role in GC opens new avenues for innovative therapeutic interventions and personalized medicine. [ABSTRACT FROM AUTHOR]

Purpose: In the Zhejiang region, research on Helicobacter pylori is lacking. The purpose of this study was to assess the extent of antibiotic resistance in H. pylori in this region, explore alternative methods for predicting the resistance patterns of H. pylori, and investigate the colonization of native gastric mucosa by other clades of H. pylori in the structure population of this bacterium. Methods: Strains were cultured under microaerobic conditions, and antimicrobial susceptibility testing (AST) was performed via agar dilution. Whole-genome sequencing (WGS) was performed via next-generation sequencing (NGS) technology. Epidemiological data including data from this study and reported articles from Zhejiang, China, were included. Further analyses based on AST, WGS, and epidemiological date include virulence genes, antibiotic resistance-related mutations, and phylogenetic trees based on 7 housekeeping genes and core-genome single nucleotide polymorphisms (SNPs). Results: The bacterial isolates in this study presented higher antibiotic resistance rates than previously reported, especially against levofloxacin and clarithromycin. The point mutation A2147G in 23 S rRNA is specific to clarithromycin resistance. Mutations at position/s 87 and/or 91 of the gyrA gene amino acid sequence are highly consistent with levofloxacin resistance highly. The point mutations C1707T in 23 S rRNA and E463K in the gyrB gene have not been previously documented in China. All the bacterial isolates belong to Asian branches in the structure population. The resistance rate to clarithromycin of isolates from hosts born after January 1, 1977 is statistically higher than that of hosts born before 1977. Conclusion: Eradication therapy based on AST results is urgently needed in Zhejiang. The point mutation A2147G in 23 S rRNA and point mutations in the gyrA gene at amino acid/s 87 and/or 91 are sufficient for predicting resistance to clarithromycin and levofloxacin, respectively. The isolate with the mutation E463K in the gyrB gene represents a significant contribution to the field. Mutations in 23 S rRNA may offer valuable insights into the dynamics of H. pylori transmission among hosts. [ABSTRACT FROM AUTHOR]

Simple Summary: Intestinal microbiota (the gut microbiome) are important for normal gut function, especially in horses which rely on gut bacteria to break down plant material in the hindgut. Understanding normal microbiota is essential to be able to assess changes that occur during disease or in response to treatments. Post-mortem studies and biopsies have found different populations in the stomach mucosa (lining) compared to feces, but the gastric fluid has not been evaluated. The objective of this study was to describe the gastric fluid microbiome of healthy horses over time, under two housing conditions, and to compare the gastric fluid to fecal microbiome of paired samples. We found that while there were fewer bacteria (taxa) identified in the gastric juice compared to feces, there was a stable population of gastric microbiota which did not vary from week-to-week under either housing condition. There was a significant difference in compositional diversity (the relatedness of taxa present) between housing conditions, with changes in the relative proportions of a few key groups when horses moved from pasture to stable. These findings are important to inform future investigations of the gastric fluid microbiota in horses. Equine gastrointestinal microbial communities vary across the gastrointestinal tract and in response to diet or disease. Understanding the composition and stability of gastric fluid microbiota in healthy horses is a prerequisite to understanding changes associated with the development of disease. The objective of this study was to describe microbial communities in the gastric fluid and feces of healthy horses longitudinally. Horses were maintained on pasture (6 weeks), stabled (5 weeks), then returned to pasture. A consistent forage diet was provided throughout. Native gastric fluid and feces were collected weekly for full-length 16S ribosomal DNA sequencing and microbial profiling analysis. Fewer taxa were identified in the gastric fluid (770) than in the feces (5284). Species richness and diversity were significantly different between sample types (p < 0.001), but not between housing locations (p = 0.3). There was a significant effect of housing and horse on the Bray–Curtis compositional diversity of gastric (p = 0.005; p = 0.009) and fecal (p = 0.001; p = 0.001) microbiota. When horses moved from pasture to stable, the relative proportions of gastric fluid Lactobacillaceae increased and Streptococcaceae decreased, while fecal Firmicutes increased and Bacteriodota decreased. Within each housing condition, there was no significant week-to-week variation in gastric (p = 0.9) or fecal (p = 0.09) microbiota. Overall, these findings support the maintenance of stable gastric and fecal microbial populations under each management condition, providing a basis for further investigation of gastric fluid microbiota in diseases of the foregut. [ABSTRACT FROM AUTHOR]

Chronic gastritis (CG) is a common inflammatory disease of chronic inflammatory lesion of gastric mucosa and in the diagnosis of gastritis in traditional Chinese medicine (TCM), CG can be classified into Cold ZHENG (syndrome in TCM) and Hot ZHENG. However, the molecular features of Cold/Hot ZHENG in CG and the mechanism of Cold/Hot herbs in formulae for CG remained unclear. In this study, we collected a transcriptomics data including 35 patients of Cold/Hot ZHENG CG and 3 scRNA-seq CG samples. And 25 formulae for CG and 89 herbs recorded in these formulae were also collected. We conduct a comprehensive analysis based on the combination of transcriptomics datasets and machine learning algorithms, to discover biomarkers for Cold/Hot ZHENG CG. Then the target profiles of the collected formulae and Cold/Hot herbs were predicted to uncover the features and biomarkers of them against Cold/Hot ZHENG CG. These biomarkers suggest that Hot ZHENG CG might be characterized by over-inflammation and exuberant metabolism, and Cold ZHENG CG showed a trend of suppression in immune regulation and energy metabolism. Biomarkers and specific pathways of Hot herbs tend to regulate immune responses and energy metabolism, while those of Cold herbs are more likely to participate in anti-inflammatory effects. Finally, the findings were verified based on public transcriptomics datasets, as well as transcriptomics and ELISA detection, taking Jin Hong tablets as a case study. Biomarkers like leptin and IL-6 together with proportions of immune cells showed significant changes after the intervention. These findings might reflect the mechanism and build a bridge between macro and micro views of Cold/Hot ZHENG as well as Cold/Hot herbs. [ABSTRACT FROM AUTHOR]

Objective: This study explored the distributions of gastric mucosal status and their links to gastric cancer within urban high‐risk individuals in China. Methods: From 2014 to 2015, a questionnaire survey was administered among individuals aged 40 to 69 years, residing for over 3 years in seven selected cities across China. Utilizing the questionnaire data, high‐risk individuals for gastric cancer were screened. These identified high‐risk individuals were invited to undergo endoscopy, followed by pathological examinations conducted for those with suspicious lesions. Prior cancer patients and those newly diagnosed with gastric cancer were excluded, and the remaining endoscopic participants were prospectively followed up until December 2021. Results: The prospective study followed 8911 individuals at high risk of gastric cancer for a median duration of 6.77 years. The incidence density of gastric cancer was 58.55 per 100,000 person‐years. At baseline, the distributions of subjects across normal gastric mucosa, gastritis/ulcer/polyp, atrophic gastritis/intestinal metaplasia, and intraepithelial neoplasia groups were 47.09%, 36.27%, 9.57%, and 7.07%, respectively. Compared with normal gastric mucosa, the hazard ratios (HRs) for gastric cancer in the other groups were 0.89 [95% confidence interval (95%CI): 0.38–2.08], 1.52 (95%CI: 0.50–4.66), and 4.63 (95%CI: 1.98–10.82). When using the 40–54 age group as the reference, the HR for 55–69 age group was 3.49 (95%CI: 1.52–7.98). Conclusion: Among high‐risk individuals with gastric cancer, the proportions of individuals exhibiting different gastric mucosal status inversely correlated with the severity of mucosal lesions, whereas the risk of gastric cancer progressively escalated with the increasing severity of mucosal lesions and advancing age. [ABSTRACT FROM AUTHOR]

Simple Summary: Channa striatus (striped murrel) is a valuable freshwater fish known for its taste and medicinal properties. Despite the advances in breeding technology, larval rearing remains a major challenge for producing high-quality seeds for commercial production. A key issue is the lack of a scientifically validated weaning protocol, resulting in high mortality during early developmental stages. After feeding different early weaning diets over 29 days, we have found that larvae fed with Artemia nauplii increased the overall larval performance during the initial exogenous feeding phase. However, constraints due to feeding solely with Artemia nauplii necessitate weaning with an artificial micro diet. By 12 dph, the performance of larvae fed with Artemia nauplii and co-feed diet (Artemia nauplii and formulated diet) showed comparable results, and by 20 dph, the larvae fed with protease supplemented formulated micro diet showed better performance compared to other treatments. Therefore, this study gives an insight for standardizing weaning protocol for C. striatus larvae based on the effects of different early weaning diets, which positively enhances survival and growth of the Channa striatus larvae. The present study was carried out to evaluate the survival, growth, and digestive ontogeny of C. striatus larvae fed with different experimental diets from 4 days post-hatch (dph) to 32 dph at three-day intervals. A total of 24,000 larvae, with 1600 larvae per tank in triplicate and an initial mean weight of 0.64 ± 0.01 mg at 4 days post hatch (dph) were subjected to five different early weaning diets, namely Artemia nauplii (T1), co-feed diet comprising Artemia nauplii and formulated micro diet (T2), formulated micro diet (T3), formulated micro diet with protease supplementation (T4), and a commercial diet (T5). All the early weaning diets significantly affected the survival, growth, and ontogeny of the digestive system. Initially at 8 dph, C. striatus fed with T1 showed better survival and growth performance compared to other treatments. By 12 dph, the larvae fed with T1 and T2 showed similar results in terms of survival and growth performance, outperforming other treatments. However, the larvae fed with T2 and T4 outperformed T1 in survival and growth performance at 16 dph. By 24–32 dph, the larvae fed with all treatments met the basic nutritional needs for survival, with T4 fed larvae showing better growth compared to other treatments. At the end of the trial, cumulative mortality was lowest in larvae fed with T1 and highest in the larvae fed with T3 and T5. Similarly, the larvae fed with T4 showed significantly higher weight gain, specific growth rate (SGR), and average daily growth (ADG), while T1 fed larvae exhibited better feed conversion ratio (FCR) and protein efficiency ratio (PER). The enzyme activity fluctuated throughout the experimental duration. Lavae fed with T1 and T2 showed higher enzyme activities initially. However, T4 fed larvae showed higher trypsin and chymotrypsin specific activity at 16 dph along with well-developed intestinal folds with dense microvilli, higher pepsin-specific activity at 20 dph onwards with fully developed gastric glands and thicker gastric mucosal epithelium, and higher amylase and lipase activity at 16 dph with large and prominent zymogen granules in the exocrine pancreas. Peaking at 4 dph, the activity of protein metabolic enzymes (AST and ALT) sharply declined at 8 dph and increased until 32 dph. Larvae fed with T1 showed higher AST and ALT activity along with increased lipid deposits, followed by those fed with T2 and the larvae fed with T4 showing higher activity without fat accumulation but significantly lower than those fed T1 and T2. From the present research findings, it is recommended to initiate weaning for Channa striatus larvae with Artemia nauplii (from 4 dph to 8 dph) followed by a co-feeding regime (Artemia nauplii and formulated diet) between 9 and 16 dph and transition to protease-supplemented micro diet (T4) from 17 dph onwards. [ABSTRACT FROM AUTHOR]

The misuse of antibiotics has led to high levels of drug-resistance in specific pathogens, promoting the search of molecules from different natural sources or the design of novel drug candidates. Medicinal and edible plants are a rich source of bioactive compounds, in particular those of polyphenol class. In the present work, we screen the antimicrobial properties of an aqueous extract prepared from the leaves of Ugni molinae (Turz) against a panel of pathogenic bacteria strains formed by Helicobacter pylori (ATCC 43504), Listeria monocytogenes (ATCC 7644), Staphylococcus aureus (ATCC 9144), Escherichia coli (ATCC 11775), and Salmonella enterica (ATCC 13076). Preliminary fast HPLC-micro fractionation allows the identification of potential urease inhibitors using high throughput urea-phenol microplate assay. Afterwards, preparative fractionation by Centrifugal Partition Chromatography (CPC) allow to select the specific bioactive fractions. A combination of antimicrobial tests, enzyme assays and molecular docking resulted in the identification by HPLC-MS/MS of two quercetin-O-(6"-O-galloyl)-hexosides as the most dominant compounds in the active CPC-fractions. These bioactive compounds were quercetin-3-O-(6"-O-galloyl)-8-galactopyranoside (hyperin 6"-gallate) and quercetin-3-O-ß-D-(6"-O-galloyl)- ß-glucopyranoside (tellimoside). The molecular docking evaluation revealed that hyperin-6"-gallate enter the binding site of urease and bind in through pi-cation, pi-pi, and H-bond interactions. In concordance with the in-silico assay, the CPC fraction containing this compound has the lowest values of IC50 for Jack bean (0.41 ± 0.08 µg/mL) and Helicobacter pylori (0.28 ± 0.08 µg/mL) ureases, respectively. Moreover, Label-Free Microscale Thermophoresis (MST) analysis suggest that this flavonoid forms a complex with urease, even inducing protein aggregation. In conclusion, Ugni molinae leaves has potent anti-urease flavonoids that can contribute to significantly reduce the acclimation of H. pylori in the acidic environmental of gastric mucosa. [ABSTRACT FROM AUTHOR]

Growth factor receptor bound protein 7 (GRB7) is reportedly upregulated in human gastric cancer (GC), which is closely associated with tumor progression and prognosis. However, the mechanism underlying its dysregulation in GC remains poorly understood. In this study, we found that GRB7 overexpression was associated with Helicobacter pylori (H. pylori) infection. GC cells (AGS and MGC-803) infection assays revealed that this upregulation was mediated by the transcription factor STAT3, and activation of STAT3 by H. pylori promoted GRB7 expression in infected GC cells. Moreover, CagA, the key virulence factor of H. pylori, was found involved in STAT3-mediated GRB7 overexpression. The overexpressed GRB7 further promoted GC cell proliferation, migration, and invasion by activating ERK signaling. Mice infection was further used to investigate the action of GRB7. In H. pylori infection, GRB7 expression in mice gastric mucosa was elevated, and higher STAT3 and ERK activation were also detected. These results revealed GRB7-mediated pathogenesis in H. pylori infection, in which H. pylori activates STAT3, leading to increased GRB7 expression, then promotes activation of the ERK signal, and finally enhances malignant properties of infected cells. Our findings elucidate the role of GRB7 in H. pylori-induced gastric disorders, offering new prospects for the treatment and prevention of H. pylori-associated gastric carcinogenesis by targeting GRB7. [ABSTRACT FROM AUTHOR]

Crohn's disease (CD) is a chronic inflammatory bowel condition with increasing global incidence. Diagnosing CD is challenging and requires close collaboration between clinicians and pathologists due to the lack of specific diagnostic criteria. Histologically, CD is characterized by transmural inflammation, crypt distortion, metaplasia, and granulomas, although granulomas are not always present. Schaumann bodies (SB), initially described in sarcoidosis, are rare in CD but have been reported in about 10% of cases. This case report presents a 4-year-old female with chronic hemorrhagic diarrhea, severe anemia, and elevated inflammatory markers. Endoscopic and histological evaluations suggested CD, with the presence of SB in the gastric mucosa. Further investigations ruled out sarcoidosis, confirming a diagnosis of multi-segmental, very early onset CD with atypical histological features. SB are inclusions composed of calcium carbonate crystals and conchoid bodies, typically found within giant cells. The presence of SB in the mucosa is rare, limiting their diagnostic significance in endoscopic biopsies. Differential diagnosis should exclude other granulomatous diseases such as intestinal tuberculosis and sarcoidosis. This case highlights the importance of considering SB in the diagnosis of CD, particularly in pediatric patients. [ABSTRACT FROM AUTHOR]

This document discusses a new database that contains 520 studies on the carcinogenicity data of 238 pharmaceuticals across 14 ATC classifications. The database includes non-clinical animal studies and human information for approved drugs, and can be used for correlation and concordance analyses. It provides insights into the tumorigenic potential of structural analogues and includes information on species, strain sensitivities, and affected organs/tissues. The authors emphasize the importance of repeat-dose toxicity studies in identifying potential concerns regarding tumorigenic potential. The database also includes information on the incidence and severity of effects observed in these studies, such as hyperplasia and neoplastic changes, which are relevant in assessing the carcinogenicity of pharmaceuticals. [Extracted from the article]

Helicobacter pylori (H. pylori) is a bacterial pathogen that exclusively colonizes the human gastric mucosa and can cause persistent infection. In this process, H. pylori employs various strategies to avoid recognition by the human immune system. These range from passive defense strategies (e.g., altered LPS or flagellin structures) that prevent recognition by pattern recognition receptors (PRRs) to more active approaches, such as inhibition of IL-2 secretion and proliferation of T cells via VacA. Despite the growing evidence that H. pylori actively manipulates the human immune system for its own benefit, the direct interaction of H. pylori with immune cells in situ is poorly studied. Here, we present a novel intravital imaging model of the murine stomach gastric mucosa and show for the first time the in situ recruitment of neutrophils during infection and a direct H. pylori-macrophage interaction. For this purpose, we applied multiphoton intravital microscopy adapted with live drift correction software (VivoFollow) on LysM-eGFP and CX3CR1-eGFP reporter mice strains in which specific subsets of leukocytes are fluorescently labeled. Multiphoton microscopy is proving to be an excellent tool for characterizing interactions between immune cells and pathogens in vivo. Author summary: This study focuses on the dynamics of H. pylori infection and its interaction with myeloid immune cells, using an innovative in vivo multiphoton imaging approach to observe real-time events in the infected gastric mucosa. In contrast to conventional methods, this novel technique allows us to dynamically investigate the host immune response. Our results show the spatio-temporal distribution of neutrophils and the internalization of H. pylori by macrophages over time. Using intravital multiphoton microscopy enhanced with live drift correction software and utilizing LysM-eGFP and CX3CR1-eGFP reporter mice, we established an intravital imaging model for the gastric mucosa of mice. Notably, we observe a significant increase in neutrophil infiltration into the gastric submucosa during early infection, indicating a rapid response of the innate immune system within the gastric crypts. However, in the chronic infection phase, a contrasting decrease in neutrophil influx is seen, indicating an adaptive innate immune response with fewer neutrophils infiltrating the tissue at an increased rate. Importantly, our data suggest that H. pylori is dependent on macrophages to proliferate and colonize the gastric mucosa during chronic infection. [ABSTRACT FROM AUTHOR]

Objective: Unusual clinical course. Background: The finding of pneumoperitoneum frequently leads to operative management for diagnosis and treatment. The etiology of pneumoperitoneum includes perforated viscus, such as perforated peptic ulcers, small or large intestinal perforations, appendicitis, and complicated sigmoid diverticulitis. We describe the preoperative, intraoperative, and postoperative course of a patient with perforated Meckel's diverticulitis presenting with pneumoperitoneum. This unusual presenting finding highlights that Meckel's diverticulum should be included in the differential diagnosis in adolescents and young adults presenting with pneumoperitoneum. Case Report: We describe a case of an 18-year-old male who presented with 1 day of abdominal pain, found to have pneumoperitoneum during workup, attributed to perforated Meckel's diverticulum. CT scans of the abdomen and pelvis were performed, confirming pneumoperitoneum, an inflamed segment of distal ileum, and a non-visualized appendix, which made the diagnosis difficult. Perforated Meckel's diverticulum, likely due to infection, was confirmed by diagnostic laparoscopy. The Meckel's diverticulum was then exteriorized and removed by segmental small bowel resection with primary anastomosis. The final pathology report confirmed perforated Meckel's diverticulum with gastric oxyntic-type mucosa. Conclusions: This case illustrates an uncommon presentation of Meckel's diverticulum in an adolescent with pneumoperitoneum. Pneumoperitoneum requires broadening the diagnosis to include other causes, including Meckel's diverticulum, especially in the setting of an acute abdomen. This case highlights that a high index of suspicion should be kept for Meckel's diverticulum, even in adolescents and young adults with pneumoperitoneum. [ABSTRACT FROM AUTHOR]

Background: Recent studies have suggested an association between H. pylori and metabolic-disfunction associated fatty liver disease (MASLD). However, epidemiologic studies have yielded inconsistent results. We aim to evaluate the association of H. pylori and G-allele PNPLA3 in MASLD diagnosis, and markers of severity. Methods: A multi-center cross-sectional study was conducted. A total 224 functional dyspepsia (FD) patients cohort who underwent gastroscopy was selected. Biochemical, clinical parameters, ultrasound, FIB-4 score, LSM by VCTE, gastric biopsies, H. pylori status, and rs738409 PNPLA3 were evaluated. A second retrospective cohort of 86 patients with biopsy-proven MASLD who underwent gastroscopy with gastric biopsies was analyzed. Results: In the FD cohort MASLD was observed in 52%, and H. pylori-positive in 51%. H. pylori infection was associated with MASLD prevalence, but in multivariate analyses adjusted for G-allele PNPLA3, it became not significant. Then in MASLD-only dyspeptic cohort, H. pylori infection was significantly linked to elevated serum AST levels and increased liver stiffness measurements, suggesting a potential role in liver injury and fibrosis. Histopathological analysis in biopsy-proven MASLD patients further supported these findings, showing a significant association between H. pylori infection and increased NAS score, fibrosis stage, and prevalence of MASH. Notably, the combination of H. pylori infection and G-allele PNPLA3 appeared to exacerbate MASLD severity beyond individual effects. Conclusions: Our results suggest that H. pylori infection may play a role in the progression of liver injury and fibrosis in patients with MASLD, especially in those with specific genetic predispositions. [ABSTRACT FROM AUTHOR]

Helicobacter pylori is one of the most common bacterial pathogens worldwide and the main etiological agent of numerous gastric diseases. The frequency of multidrug resistance of H. pylori is growing and the leading factor related to this phenomenon is its ability to form biofilm. Therefore, the establishment of a proper model to study this structure is of critical need. In response to this, the aim of this original article is to validate conditions of the optimal biofilm development of H. pylori in monoculture and co-culture with a gastric cell line in media simulating human fluids. Using a set of culture-based and microscopic techniques, we proved that simulated transcellular fluid and simulated gastric fluid, when applied in appropriate concentrations, stimulate autoaggregation and biofilm formation of H. pylori. Additionally, using a co-culture system on semi-permeable membranes in media imitating the stomach environment, we were able to obtain a monolayer of a gastric cell line with H. pylori biofilm on its surface. We believe that the current model for H. pylori biofilm formation in monoculture and co-culture with gastric cells in media containing host-mimicking fluids will constitute a platform for the intensification of research on H. pylori biofilms in in vitro conditions that simulate the human body. [ABSTRACT FROM AUTHOR]

This study aimed to analyze the structure of polysaccharides from eight different Dendrobium species and their protective effects on gastric mucosa. Ultraviolet (UV) analysis showed that the contents of eight polysaccharides ranged from 51.89 ± 6.91% to 80.57 ± 11.63%; the degree of acetylation ranged from 0.17 ± 0.03 to 0.48 ± 0.03. High-performance liquid chromatography (HPLC) results showed that these polysaccharides were mainly composed of mannose (Man) and glucose (Glc) with a small amount of galactose (Gal) and arabinose (Ara), and the monosaccharide ratios of different Dendrobium species were different. High-performance size exclusion chromatography—multi angle light scattering—refractive index detector (HPSEC-MALS-RID) showed that the molecular weight (Mw) of all Dendrobium polysaccharides was >1 × 105 Da; D. huoshanense had the lowest molecular weight. Subsequently, an ethanol injured GES-1 cell model was constructed to evaluate the gastric mucosal protective potential of polysaccharides from eight different Dendrobium species. The results showed that the protective effect of the low concentration 50 μg/mL DHP treatment group was similar to that of the control group (p > 0.05), and the cell viability could reach 97.32% of that of the control group. Based on the polysaccharide composition, different kinds of Dendrobium have different degrees of migration and repair effects on GES-1 damaged cells, and the effect of DHP is slightly better than that of other varieties (83.13 ± 1.05%). Additionally, Dendrobium polysaccharides alleviated ethanol-induced oxidative stress and inflammatory response in gastric mucosal cells by enhancing the activity of antioxidant enzymes (superoxide dismutase, glutathione peroxidase, catalase) and reducing the levels of malondialdehyde and reactive oxygen species. Overall, DHP can most effectively protect gastric mucosa. These findings enhance our understanding of the relationship between the structure and biological activity of Dendrobium polysaccharides, providing a foundation for the quality control of Dendrobium. Furthermore, these findings offer theoretical support for the development of Dendrobium polysaccharides as nutraceuticals to treat digestive system diseases. [ABSTRACT FROM AUTHOR]

Background: Helicobacter pylori infects the stomach and/or small intestines in more than half of the human population. Infection with H. pylori is the most common cause of chronic gastritis, which can lead to more severe gastroduodenal pathologies such as peptic ulcer, mucosa-associated lymphoid tissue lymphoma, and gastric cancer. H. pylori infection is particularly concerning in Colombia in South America, where > 80% of the population is estimated to be infected with H. pylori and the rate of stomach cancer is one of the highest in the continent. Results: We compared the antimicrobial susceptibility profiles and short-read genome sequences of five H. pylori isolates obtained from patients diagnosed with gastritis of varying severity (chronic gastritis, antral erosive gastritis, superficial gastritis) in Pereira, Colombia sampled in 2015. Antimicrobial susceptibility tests revealed the isolates to be resistant to at least one of the five antimicrobials tested: four isolates were resistant to metronidazole, two to clarithromycin, two to levofloxacin, and one to rifampin. All isolates were susceptible to tetracycline and amoxicillin. Comparative genome analyses revealed the presence of genes associated with efflux pump, restriction modification systems, phages and insertion sequences, and virulence genes including the cytotoxin genes cagA and vacA. The five genomes represent three novel sequence types. In the context of the Colombian and global populations, the five H. pylori isolates from Pereira were phylogenetically distant to each other but were closely related to other lineages circulating in the country. Conclusions: H. pylori from gastritis of different severity varied in their antimicrobial susceptibility profiles and genome content. This knowledge will be useful in implementing appropriate eradication treatment regimens for specific types of gastritis. Understanding the genetic and phenotypic heterogeneity in H. pylori across the geographical landscape is critical in informing health policies for effective disease prevention and management that is most effective at local and country-wide scales. This is especially important in Colombia and other South American countries that are poorly represented in global genomic surveillance studies of bacterial pathogens. [ABSTRACT FROM AUTHOR]

Introduction: Many drugs are irritating to the gastric mucosa and induce gastric erosion and when these side effects are coupled with additional parameters, such as bacterial infection, stress, and gastric pH, these together induce gastric ulcer. The present study aimed to evaluate the gastric erosion effects of chloroquine using mice models. Methods: A total of 20 mice were used for this study, divided into two groups of 10 each; the control group was administered only standard food and water, and the chloroquine group was given standard food with water with additional chloroquine solution of 1.2 mg/kg daily orally for a month. The stomachs were dissected and sliced for histological staining and analysis. Results: Chloroquine has remarkably induced tissue degeneration and villi sloughing alongside white blood cell infiltration with patchy areas of stomach erosion compared to the normal architecture of the stomach tissue of the control group. Conclusion: Chloroquine-induced gastric erosion with potential involvement of the many regions of the stomach reaching deep tissue layers. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to optimize the formulation of a C60-modified self-microemulsifying drug delivery system loaded with triptolide (C60-SMEDDS/TP) and evaluate the cytoprotective effect of the C60-SMEDDS/TP on normal human cells. Results: The C60-SMEDDS/TP exhibited rapid emulsification, an optimal particle size distribution of 50 ± 0.19 nm (PDI 0.211 ± 0.049), and a near-neutral zeta potential of −1.60 mV. The release kinetics of TP from the C60-SMEDDS/TP exhibited a sustained release profile and followed pseudo-first-order release kinetics. Cellular proliferation and apoptosis analysis indicated that the C60-SMEDDS/TP (with a mass ratio of TP: DSPE-PEG-C60 = 1:10) exhibited lower toxicity towards L02 and GES-1 cells. This was demonstrated by a higher IC50 (40.88 nM on L02 cells and 17.22 nM on GES-1 cells) compared to free TP (21.3 nM and 11.1 nM), and a lower apoptosis rate (20.8% on L02 cells and 26.3% on GES-1 cells, respectively) compared to free TP (50.5% and 47.0%) at a concentration of 50 nM. In comparison to the free TP group, L02 cells and GES-1 cells exposed to the C60-SMEDDS/TP exhibited a significant decrease in intracellular ROS and an increase in mitochondrial membrane potential (ΔψM). On the other hand, the C60-SMEDDS/TP demonstrated a similar inhibitory effect on BEL-7402 cells (IC50 = 28.9 nM) and HepG2 cells (IC50 = 107.6 nM), comparable to that of the free TP (27.2 nM and 90.4 nM). The C60-SMEDDS/TP group also exhibited a similar intracellular level of ROS and mitochondrial membrane potential compared to the SMEDDS/TP and free TP groups. Method: Fullerenol-Grafted Distearoyl Phosphatidylethanolamine-Polyethylene Glycol (DSPE-PEG-C60) was synthesized and applied in the self-microemulsifying drug delivery system. The C60-SMEDDS/TP was formulated using Cremophor EL, medium-chain triglycerides (MCT), PEG-400, and DSPE-PEG-C60, and loaded with triptolide (TP). The toxicity and bioactivity of the C60-SMEDDS/TP were assessed using normal human liver cell lines (L02 cells), normal human gastric mucosal epithelial cell lines (GES-1 cells), and liver cancer cell lines (BEL-7402 cells and HepG2 cells). The production of reactive oxygen species (ROS) after the C60-SMEDDS/TP treatment was assessed using 2′,7′-dichlorofluorescein diacetate (DCFDA) staining. The alterations in mitochondrial membrane potential (ΔψM) were assessed by measuring JC-1 fluorescence. Conclusions: The cytoprotection provided by the C60-SMEDDS/TP favored normal cells (L02 and GES-1) over tumor cells (BEL-7402 and HepG2 cells) in vitro. This suggests a promising approach for the safe and effective treatment of TP. [ABSTRACT FROM AUTHOR]

Endoscopic resection (ER)–a minimal invasive procedure, compared to surgical gastrectomy, with the advantage of preserving the entire stomach and maintaining the patient’s quality of life–is a widely used curative treatment for early gastric cancers (EGCs). Despite its advantages, such as the preservation of the whole stomach, a large area of the gastric mucosa with histologic changes such as atrophy and intestinal metaplasia remains after ER, and so does the risk of metachronous gastric cancers (MGCs). Therefore, regular surveillance endoscopy after curative ER of EGCs is important so that MGCs are detected early and so minimally invasive ER remains a treatment option. To date, the optimal interval for surveillance endoscopy after curative ER of EGCs has not been established. Therefore, this review summarizes the results of the published studies on this topic with the aim of establishing the optimal surveillance interval for early identification of MGCs. Based on my review, the median timing of MGC occurrence is within 3 years, and reports suggest biannual endoscopy during the first 3 years; however, the evidence suggests that individual patient characteristics may influence the risk of MGCs. Therefore, stratified endoscopic strategies for surveillance based on patient characteristics, such as age, family history of gastric cancer, synchronous gastric lesions, and corpus intestinal metaplasia, should be applied. [ABSTRACT FROM AUTHOR]

Aim The imaging of Meckel's diverticulum (MD) is based of accumulation of Tc-99m pertechnetate in the ectopic gastric mucosa (EGM) content. Although the diagnostic accuracy of this imaging modality is high, there are some overlap patients with coexisting gastrointestinal bleeding and false positive causes hampering diagnostic power. The aim of this study was to evaluate the possible contribution of single-photon emission computed tomography/computed tomography (SPECT/CT) in EGM-MD diagnosis and to determine the indication of this additional imaging modality. Materials and Methods Fifty-two pediatric patients (24 girls, 28 boys; mean age: 8.06 ± 5.22 years old) who have suspicion of MD and referred for scintigraphy were evaluated retrospectively. Additional SPECT/CT were performed to selected five cases among the group. The results of the scintigraphy as well as SPECT/CT were compared with endoscopy, pathology, and/or follow-up results. Results There were 9 patients with equivocal study results, 12 positive results, and the others were considered negative MD scintigraphy. One patient was out of follow-up and 10 patients underwent surgery. Only one single patient was negative during surgery but scintigraphy was also negative. The diagnostic sensitivity, specificity, and accuracy were 100, 95, and 96%, respectively. Among five patients with SPECT/CT results one patient was diagnosed by only SPECT/CT who had EGM in duplication cyst, one equivocal patient was diagnosed as descending colon bleeding, and one patient's lesion was clearly delineated by SPECT/CT. Conclusion SPECT/CT has clear advantage over standard planar scintigraphy imaging in EGM-MD determination. This modality might decrease equivocal and false positive results but this issue has to be addressed with further studies. [ABSTRACT FROM AUTHOR]

The resistance of Helicobacter pylori (H. pylori) has increased in recent years, prompting a trend in the research and development of new drugs. In our study, three derivatives (JF-1, JF-2, and JF-3) were synthesized using 6-gingerol as the main component, while JF-4, containing both 6-gingerol and 6-shogaol as the main components, was extracted from dried ginger. The minimum inhibitory concentrations (MICs), determined using the ratio dilution method, were 80 μg/mL for JF-1, 40 μg/mL for JF-2, 30 μg/mL for JF-3, 40 μg/mL for JF-4, 60 μg/mL for 6-gingerol standard (SS), and 0.03 μg/mL for amoxicillin (AMX). After treating H. pylori-infected mice, the inflammation of the gastric mucosa was suppressed. The eradication rate of H. pylori was 16.7% of JF-3 low-dose treatment (LDT), 25.0% of JF-3 high-dose treatment (HDT), 16.7% of JF-4 LDT, 16.7% of JF-4 HDT, 30% of SS LDT, 50% of SS HDT, and 36.4% of the positive control group (PCG). The levels of gastrin, somatostatin (SST), IFN-γ, IL-4, and IL-8 were significantly recovered in the JF-3 and JF-4 administration groups, but the effect was stronger in the high-dose group. These results demonstrate that 6-gingerol and its derivatives have significant anti-Helicobacter pylori effects and are promising potential treatments for H. pylori infection. [ABSTRACT FROM AUTHOR]

Background: H. pylori infection has been recognized as a type 1 carcinogen of the gastric malignancy; therefore, early diagnosis and treatment are the corner stone of eradication. Recent findings have also shown that atrophy and intestinal metaplasia remain after successful eradication, which moderately increases the risk of gastric cancer compared with those who have never infected, so the evaluation of gastric mucosa during gastroscopy is important. Aims: We aimed to describe and summarize the reliable literature and proposed features of H. pylori infection status and gastritis in research on newly developed endoscopic models that influence clinical practice. In the result, conventional white light endoscopic, image‐enhanced endoscopic models, and studies related to the Kyoto classification of gastritis were searched and reviewed. Results: Kyoto classification of gastritis and modified Kyoto classification scoring model for gastritis using conventional white light image (CWLI) endoscopy is an effective tool for evaluating current H. pylori infection status, past infections, eradications, noninfections, and pre‐cancerous conditions. This model is widely used, low cost, and time‐efficient, and is supported by recent findings. Advanced image‐enhanced endoscopic models combined with magnifying endoscopy provide more clear endoscopic features for H. pylori infection status and early gastric cancer. Conclusion: According to H pylori infection status, endoscopic prediction of gastric mucosal surface architecture analysis is possible, which influences clinical management. Endoscopic models might lead us to accurate and early diagnose of H. pylori infection status and may not be effective only for the eradication of H. pylori infection but also in the detection of early gastric cancer status. [ABSTRACT FROM AUTHOR]

Gastric cancer (GC) is a complex disease with various etiologies. While Helicobacter pylori infection is still one of the leading risk factors for GC, increasing evidence suggests a link between GC and other infective agents such as Epstein Bar Virus (EBV). EBV-associated gastric cancer (EBVaGC) is now recognized as a distinct subgroup of GC, and the complex interactions between the virus and gastric mucosa may influence its development. A recent integrative analysis of the genome and proteome of GC tissues by The Cancer Genome Atlas project has identified EBVaGC as a specific subtype characterized by PIK3CA and ARID1A mutations, extensive DNA hyper-methylation, and activation of immune signaling pathways. These molecular characteristics are markers of the unique molecular profile of this subset of GC and are potential targets for therapy. This review aims to provide an overview of the current knowledge on EBVaGC. It will focus on the epidemiology, clinic-pathological features, and genetic characteristics of EBVaGC. Additionally, it will discuss recent data indicating the potential use of EBV infection as a predictive biomarker of response to chemotherapy and immune checkpoint inhibitors. The review also delves into potential therapeutic approaches for EBVaGC, including targeted therapies and adoptive immunotherapy, highlighting the promising potential of EBV as a therapeutic target. [ABSTRACT FROM AUTHOR]

Objectives: This study aimed to observe the intervention of Weizhuan'an prescription on rats with precancerous lesions of gastric cancer (PLGC) as well as its regulation on gastric mucosal microflora and inflammatory factors and explore the pharmacodynamic mechanisms of Weizhuan'an Formula. Methods: The rats were classified into the blank control group (BCG); low-, medium-, and high-dose groups of Weizhuan'an prescription (LDG, MDG, and HDG, respectively); and natural recovery group (NRG) at random. The rats in the traditional Chinese medicine (TCM) group were given corresponding doses of Weizhuan'an formula, while the rats in the NRG and BCG were given an equivalent volume of distilled water for 12 weeks. After that, gastric mucosa samples of rats were collected to observe the general and pathological changes in the gastric mucosa; the changes in gastric mucosal microflora were detected by 16S rDNA amplicon sequencing, and the inflammatory factors were analyzed by cytokine antibody microarray and Western blotting. Results: The results suggest that compared with the BCG, the pathology of gastricmucosa and gastricmucosal microflora and inflammatory factors in rats with PLGC have changed significantly, while Weizhuan'an formula effectively improved them, especially in the MDG and HDG (p < 0.05). Compared with the NRG, the abundance of probiotics such as Lactobacillus and Veillonella were increased, while the abundance of pathogens such as Proteobacteria and Pseudomonas was decreased (p < 0.05, p < 0.01), and the relative contents of IL-2, IL-4, IL-13, and MCP-1 in gastric mucosa were decreased (p < 0.05). Moreover, it can upregulate the DNA-binding transcriptional regulator, ABC type multidrug transport system, and related enzymes and affect the signaling pathways such as viral protein interaction with cytokine and cytokine receptor and T cell receptor signaling pathway significantly (p < 0.05, p < 0.01), which can promote drug absorption and utilization and repair damaged gastric mucosa. Conclusion: The study confirmed that Weizhuan'an prescription can treat rats with PLGC by regulating gastric mucosal microflora and inflammatory factors. [ABSTRACT FROM AUTHOR]

Gastrointestinal mucosal surface is frequently under challenge due to it's the large surface area and most common entry of microbes. IL-37, an antiinflammatory cytokine, regulates local and systemic host immunity. H. pylori infection leads to the inhibition of IL-37 in the gastric mucosa, contributing to heightened mucosal inflammation and destruction, thereby facilitating increased proliferation of H. pylori. Food allergy, due to immune dysregulation, also contribute to GI injury. On the other hand, elevated levels of IL-37 observed in gastric cancer patients align with reduced host immunity at the cellular and humoral levels, indicating that IL-37 may contribute to the development of gastric cancer via suppressing pro-inflammatory responses. While IL-37 provides protection in an IBD animal model, the detection of highly produced IL-37 in IBD patients suggests a stage-dependent role, being protective in acute inflammation but potentially exacerbates the development of IBD in chronic conditions. Moreover, elevated colonic IL-37 in CRC correlates with overall survival time and disease time, indicating a protective role for IL-37 in CRC. The differential regulation and expression of IL-37 between upper- and lower-GI organs may be attributed to variations in the microbial flora. This information suggests that IL-37 could be a potential therapeutic agent, depending on the stage and location. [ABSTRACT FROM AUTHOR]

Cases and studies of protruding early gastric cancer (EGC) combined with spontaneous bleeding are relatively rare. The current study present a female patient aged 70 to 75 years old with hemorrhagic shock caused by spontaneous bleeding from EGC type 0-Isp, which was successfully cured by rapid emergency endoscopic submucosal dissection (ESD). [ABSTRACT FROM AUTHOR]

The urease enzyme is recognized as a valuable therapeutic agent for treating the virulent Helicobacter pylori bacterium because of its pivotal role in aiding the colonization and growth of the bacterium within the gastric mucosa. In order to control the harmful consequences of bacterial infections, urease inhibition presents itself as a promising and effective approach. The current research aimed to synthesize pyridylpiperazine-based carbodithioate derivatives 5a-5n and 7a-7n that could serve as potential drug candidates for preventing bacterial infections through urease inhibition. The synthesized carbodithioate derivatives 5a-5n and 7a-7n were explored to assess their ability to inhibit the urease enzyme after their structural explication by gas chromatography-mass spectrometry (GC-MS). In the in vitro evaluation with thiourea as a standard drug, it was observed that all the synthesized compounds exhibited significant inhibitory activity compared to the reference drug. Among the compounds tested, 5j (bearing an o-tolyl moiety) emerged as the most effective inhibitor, displaying strong urease inhibition with an IC50 value of 5.16 ± 2.68 pM. This IC50 value is notably lower than that of thiourea (23 ± 0.03 pM), indicating the significantly most potent potential of inhibition. In molecular docking of 5j within the active site of urease, numerous noteworthy interactions were identified. [ABSTRACT FROM AUTHOR]

Objectives: We aimed to identify predictive markers for metachronous gastric cancer (MGC) in early gastric cancer (EGC) patients curatively treated with endoscopic submucosal dissection (ESD). Materials and Methods: From EGC patients who underwent ESD, bulk RNA sequencing was performed on non‐cancerous gastric mucosa samples at the time of initial EGC diagnosis. This included 23 patients who developed MGC, and 23 control patients without additional gastric neoplasms for over 3 years (1:1 matched by age, sex, and Helicobacter pylori infection state). Candidate differentially‐expressed genes were identified, from which biomarkers were selected using real‐time quantitative polymerase chain reaction and cell viability assays using gastric cell lines. An independent validation cohort of 55 MGC patients and 125 controls was used for marker validation. We also examined the severity of gastric intestinal metaplasia, a known premalignant condition, at initial diagnosis. Results: From the discovery cohort, 86 candidate genes were identified of which KDF1 and CDK1 were selected as markers for MGC, which were confirmed in the validation cohort. CERB5 and AKT2 isoform were identified as markers related to intestinal metaplasia and were also highly expressed in MGC patients compared to controls (p < 0.01). Combining these markers with clinical data (age, sex, H. pylori and severity of intestinal metaplasia) yielded an area under the curve (AUC) of 0.91 (95% CI, 0.85‐0.97) for MGC prediction. Conclusion: Assessing biomarkers in non‐cancerous gastric mucosa may be a useful method for predicting MGC in EGC patients and identifying patients with a higher risk of developing MGC, who can benefit from rigorous surveillance. [ABSTRACT FROM AUTHOR]

Background: Helicobacter pylori (H. pylori) infection is critical in the development and occurrence of gastric cancer. H. pylori secretes gamma-glutamyl transferase (GGT), which affects energy metabolism and histone methylation in mesenchymal stem cells. However, its effect on human gastric epithelial cells remains unclear. This study aimed to investigate the effects of GGT on energy metabolism and histone methylation in gastric epithelial cells and determine its role in the development and progression of H. pylori-induced gastric cancer. Methods: A GGT knockout H. pylori strain and mouse gastric cancer model were constructed, and alpha-ketoglutarate (α-KG) was added. The underlying mechanism was investigated using proteomics, immunohistochemistry, Western blotting, and other experimental assays. Results: H. pylori can colonize the host's stomach and destroy the gastric epithelium. GGT secreted by H. pylori decreased the concentration of glutamine in the stomach and increased H3K9me3 and H3K27me3 expression, which promoted the proliferation and migration of gastric epithelial cells. Additionally, α-KG reversed this effect. GGT increased the tumorigenic ability of nude mice. GGT, secreted by H. pylori, promoted the expression of ribosomal protein L15 (RPL15), while GGT knockout and supplementation with α-KG and trimethylation inhibitors reduced RPL15 expression and Wnt signaling pathway expression. Conclusions: H. pylori secreted GGT decreased the expression of glutamine and α-KG in gastric epithelial cells, increased the expression of histones H3K9me3 and H3K27me3, and activated the Wnt signaling pathway through RPL15 expression, ultimately changing the biological characteristics of the gastric epithelium and promoting the occurrence of gastric cancer. Altered energy metabolism and histone hypermethylation are important factors involved in this process. [ABSTRACT FROM AUTHOR]

Galectins are β-galactoside-binding animal lectins involved in various biological functions, such as host defense. Galectin-2 and -3 are members of the galectin family that are expressed in the stomach, including the gastric mucosa and surface mucous cells. Galectin-3 exhibits aggregation and bactericidal activity against Helicobacter pylori in a β-galactoside-dependent manner. We previously reported that galectin-2 has the same activity under neutral pH conditions. In this study, the H. pylori aggregation activity of galectin-2 was examined under weakly acidic conditions, in which H. pylori survived. Galectin-2 agglutinated H. pylori even at pH 6.0, but not at pH 5.0, correlating with its structural stability, as determined using circular dichroism. Additionally, galectin-2 binding to the lipopolysaccharide (LPS) of H. pylori cultured under weakly acidic conditions was investigated using affinity chromatography and Western blotting. Galectin-2 could bind to H. pylori LPS containing H type I, a Lewis antigen, in a β-galactoside-dependent manner. In contrast, galectin-3 was structurally more stable than galectin-2 under acidic conditions and bound to H. pylori LPS containing H type I and Lewis X. In conclusion, galectin-2 and -3 might function cooperatively in the defense against H. pylori in the stomach under different pH conditions. [ABSTRACT FROM AUTHOR]

Helicobacter pylori (H. pylori) infection is the primary risk factor for the progress of gastric diseases. The persistent stomach colonization of H. pylori is closely associated with the development of gastritis and malignancies. Although the involvement of progranulin (PGRN) in various cancer types has been welldocumented, its functional role and underlying mechanisms in gastric cancer (GC) associated with H. pylori infection remain largely unknown. This report demonstrated that PGRN was up-regulated in GC and associated with poor prognosis, as determined through local and public database analysis. Additionally, H. pylori induced the up-regulation of PGRN in gastric epithelial cells both in vitro and in vivo. Functional studies have shown that PGRN promoted the intracellular colonization of H. pylori. Mechanistically, H. pylori infection induced autophagy, while PGRN inhibited autophagy to promote the intracellular colonization of H. pylori. Furthermore, PGRN suppressed H. pyloriinduced autophagy by down-regulating decorin (DCN) through the mTOR pathway. In general, PGRN inhibited autophagy to facilitate intracellular colonization of H. pylori via the PGRN/mTOR/DCN axis. This study provides new insights into the molecular mechanisms underlying the progression of gastric diseases, suggesting PGRN as a potential therapeutic target and prognostic predictor for these disorders. [ABSTRACT FROM AUTHOR]

Programmed cell death (PCD) plays a crucial role in maintaining the normal structure and function of the digestive tract in the body. Infection with Helicobacter pylori (H. pylori) is an important factor leading to gastric damage, promoting the Correa cascade and accelerating the transition from gastritis to gastric cancer. Recent research has shown that several PCD signaling pathways are abnormally activated during H. pylori infection, and the dysfunction of PCD is thought to contribute to the development of gastric cancer and interfere with treatment. With the deepening of studies on H. pylori infection in terms of PCD, exploring the interaction mechanisms between H. pylori and the body in different PCD pathways may become an important research direction for the future treatment of H. pylori infection and H. pylori-related gastric cancer. In addition, biologically active compounds that can inhibit or induce PCD may serve as key elements for the treatment of this disease. In this review, we briefly describe the process of PCD, discuss the interaction between different PCD signaling pathways and the mechanisms of H. pylori infection or H. pylori-related gastric cancer, and summarize the active molecules that may play a therapeutic role in each PCD pathway during this process, with the expectation of providing a more comprehensive understanding of the role of PCD in H. pylori infection. [ABSTRACT FROM AUTHOR]

Helicobacter pylori infection is involved in gastric diseases such as peptic ulcer and adenocarcinoma. Approved antibiotherapies still fail in 10 to 40% of the infected patients and, in this scenario, targeted nanotherapeutics emerged as powerful allies for H. pylori eradication. Nano/microparticles conjugated with H. pylori binding molecules were developed to eliminate H. pylori by either (i) blocking essential mechanisms of infection, such as adhesion to gastric mucosa or (ii) binding and killing H. pylori through the release of drugs within the bacteria or at the site of infection. Glycan antigens (as Lewis B and sialyl-Lewis X), pectins, lectins, phosphatidylethanolamine and epithelial cell membranes were conjugated with nano/microparticles to successfully block H. pylori adhesion. Urea-coated nanoparticles were used to improve drug delivery inside bacteria through H. pylori UreI channel. Moreover, nanoparticles coated with antibodies against H. pylori and loaded with sono/photosensitizers, were promising for their application as targeted sono/photodynamic therapies. Further, non-specific H. pylori nano/microparticles, but only active in the acidic gastric environment, coated with binders to bacterial membrane, extracellular polymeric substances or to high temperature requirement A protease, were evaluated. In this review, an overview of the existing nanotherapeutics targeting H. pylori will be given and their rational, potential to counteract infection, as well as level of development will be presented and discussed. [ABSTRACT FROM AUTHOR]