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Helicobacter pylori (H. pylori , HP), recognized globally as one of the most widespread bacteria, serves as primary etiological agent for numerous gastroduodenal diseases, highlighting the urgent need to develop rapid and sensitive diagnostic method for H. pylori infection. Here, we devised a new diagnostic test that merged multiple cross displacement amplification (MCDA) with nanoparticle‐based lateral flow biosensor (LFB), termed HP‐MCDA‐LFB, to facilitate the rapid and sensitive detection of H. pylori. The whole detection workflow, which includes stages such as DNA template extraction (~15 min), MCDA pre-amplification (~40 min), and result readout (~2 min), was efficiently completed within 1 h. After optimization, the HP-MCDA-LFB assay demonstrated remarkable sensitivity in detecting H. pylori , with a detection threshold as low as 60 fg of genomic DNA (~56 copies) per microliter. Furthermore, the HP-MCDA-LFB assay also achieved a perfect specificity rate of 100%, exhibiting no cross-reactivity with non- Helicobacter isolates. Particularly, the clinical feasibility of HP-MCDA-LFB assay was validated using 40 antral mucosa samples, among which 17 tested positive for H. pylori , which was in complete agreement with the results obtained from the rapid urease test. In conclusion, the HP‐MCDA‐LFB method developed in this study is a rapid, sensitive, and specific method for diagnosing H. pylori infection, indicating great potential for H. pylori eradication therapy. [ABSTRACT FROM AUTHOR]

The Epstein-Barr viwrus (EBV) is a common herpesvirus that affects more than 90% of people worldwide. Even while EBV infections are frequently asymptomatic, they can cause autoimmune diseases and a number of cancers, especially in those with impaired immune systems. The intricate relationships between EBV and other coinfecting pathogens, including as human immunodeficiency virus (HIV), human papilloma virus (HPV), cytomegalovirus (CMV), and Plasmodium species, are examined in this study. We investigated the fundamental processes of these coinfections, their effects on the course of the disease, and their practical ramifications. The study reviewed how co-infections with EBV might modify immune responses, promote oncogenesis, and make treatment plans more challenging. In this review, we also discussed current therapeutic strategies, such as targeted molecular interventions, EBV vaccines, and adoptive T-cell therapy. The review underscores the need for more research to provide more focused and effective therapies that address the mutually reinforcing effects of numerous infections in disorders linked with EBV. [ABSTRACT FROM AUTHOR]

A recent consensus meeting (RE.GA.IN) addressed "host-related, low-prevalence gastritis": eosinophilic (EoG), lymphocytic (Hp -pos_LyG and Hp -neg_LyG), collagenous (CollG), and granulomatous gastritis (GrG). Our study evaluates their clinico-epidemiological characteristics. We extracted all patients with a diagnosis of EoG, LyG, CollG, and GrG from a clinicopathological database and compared their demographics, clinical and endoscopic characteristics, associated conditions, and clinical awareness to those of all other subjects in the database (controls). There were 1,781,005 unique patients (median age 57 years; 55.7 % female). Hispanics were overrepresented amongst those with Hp -pos_LyG. Subjects with GrG had a high prevalence of erosions and ulcers. Clinical awareness of these conditions was dismal (<1:10,000 patients). Some clinical manifestations were more common in patients with certain gastritides (e.g., vomiting and diarrhea in CollG; anemia in LyG), but none were sufficiently distinctive to suggest a clinical diagnosis. EoG was associated with EoE; LyG had a strong association with celiac disease; CollG with microscopic colitis; and GrG with Crohn disease. The diagnosis of these gastritides (between <1: in 1,000 and 1 in 5000 subjects) rests on histopathology. They remain poorly characterized and clinically neglected. Yet, their associations may herald other conditions: eosinophilic gastrointestinal diseases (EGID), celiac, and Crohn disease. Patients might benefit from increased detection and characterization. [ABSTRACT FROM AUTHOR]

Objective. This study aimed to investigate the risk factors associated with central serous chorioretinopathy (CSC) and analyze the relationship between vascular endothelial growth factor (VEGF), high‐sensitivity C‐reactive protein (hs‐CRP), erythrocyte sedimentation rate (ESR), and CSC. Methods. A total of 109 patients diagnosed with CSC (CSC group) at our ophthalmology clinic from February 2017 to February 2021 were included, with 103 volunteers from our hospital's health examination center serving as the control group. Additionally, the new multimodal imaging classification of 109 CSC patients was further divided into simple CSC (57 cases) and complex CSC (52 cases). Demographic data, underlying diseases, medical history, and medication history were collected. Levels of VEGF, hs‐CRP, and ESR were measured, and multifactorial logistic regression analysis was performed to identify factors influencing CSC. Receiver operating characteristic (ROC) curve analysis was conducted to assess the diagnostic value of VEGF, hs‐CRP, and ESR in CSC. Results. The CSC group showed a higher proportion of males, smoking history, alcohol consumption, comorbid obstructive sleep apnea, hypothyroidism, renal disease, Helicobacter pylori infection, steroid use, and shift work compared to the control group (P < 0.05). VEGF, hs‐CRP, and ESR levels were significantly higher in the CSC group than in the control group (P < 0.05). The levels of VEGF, hs‐CRP, and ESR in the complex CSC group were higher than those in the simple CSC group (P < 0.05). Male gender, shift work, Helicobacter pylori infection, hypothyroidism, elevated VEGF, hs‐CRP, and ESR were identified as risk factors for CSC (P < 0.05). The combined diagnostic value of VEGF, hs‐CRP, and ESR (area under the ROC curve: 0.886) was higher than that of individual markers (0.722, 0.728, and 0.703, respectively) (P < 0.05). Conclusion. Male gender, shift work, Helicobacter pylori infection, hypothyroidism, and elevated levels of VEGF, hs‐CRP, and ESR are risk factors for CSC. The combined use of VEGF, hs‐CRP, and ESR demonstrates higher diagnostic efficiency in identifying CSC. [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]

Helicobacter pylori (H. pylori) is a harmful bacterium that is difficult to conveniently diagnose and effectively eradicate. Chronic H. pylori infection increases the risk of gastrointestinal diseases, even cancers. Despite the known findings, more underlying mechanisms are to be deeply explored to facilitate the development of novel prevention and treatment strategies of H. pylori infection. Long noncoding RNAs (lncRNAs) are RNAs with more than 200 nucleotides. They may be implicated in cell proliferation, inflammation and many other signaling pathways of gastrointestinal cancer progression. The dynamic expression of lncRNAs indicates their potential to be diagnostic or prognostic biomarkers. In this paper, we comprehensively summarize the processes of H. pylori infection and the treatment methods, review the known findings of lncRNA classification and functional mechanisms, elucidate the roles of lncRNAs in H. pylori-related gastrointestinal cancer, and discuss the clinical perspectives of lncRNAs. [ABSTRACT FROM AUTHOR]

Helicobacter pylori infection is a well-established risk factor for the development of gastric cancer (GC). Understanding the immunopathogenesis underlying this association is crucial for developing effective preventive and therapeutic strategies. This narrative review comprehensively explores the immunopathogenesis of H. pylori-induced GC by delving into several key aspects, emphasizing the pivotal roles played by H. pylori virulence factors, including cytotoxin-associated gene A (cagA) and vacuolating cytotoxin A (vacA), blood group antigen-binding adhesin (babA), and sialic acid binding adhesin (sabA). Moreover, the review focuses on the role of toll-like receptors (TLRs) and cytokines in the complex interplay between chronic infection and gastric carcinogenesis. Finally, the study examines the association between H. pylori evasion of the innate and adaptive immune response and development of GC. A comprehensive understanding of the immunopathogenesis of H. pylori-induced GC is essential for designing targeted interventions to prevent and manage this disease. Further research is warranted to elucidate the intricate immune responses involved and identify potential therapeutic targets to improve patient outcomes. [ABSTRACT FROM AUTHOR]

Background: Chronic gastritis caused by Helicobacter pylori (Hp) infection is a common gastrointestinal disorder. Despite the high prevalence of Hp infection and chronic gastritis in the Tibetan Plateau, there is a lack of studies elucidating the influence of plateau hypoxia on Hp-induced gastritis. This study aimed to investigate the impact of high-altitude hypoxia on Hp-induced gastritis, particularly focusing on pathological manifestations and inflammatory responses. Methods: This study was conducted from July 2023 to March 2024 at the Department of Gastroenterology, Affiliated Hospital of Qinghai University. Ninety patients diagnosed with chronic gastritis were enrolled in the study and divided into four groups based on their residential altitude and Hp infection status. Data on endoscopic and pathological characteristics were collected, along with serum oxidative stress and inflammatory markers. Results: Patients with Hp gastritis exhibit distinctive features in the gastric mucosa, including diffuse erythema, enlarged folds, and white turbid mucus during endoscopy. Notably, individuals with Hp gastritis at high altitudes show a higher prevalence of diffuse erythema and enlarged folds. Pathological analysis reveals that these patients have elevated gastric mucosal inflammation scores and increased chronic and active inflammation. Furthermore, individuals with Hp gastritis at high altitudes demonstrate elevated levels of serum TNF-α, IL-1β, IL-6, and MDA, as well as reduced serum SOD and GSH-Px activities. Conclusions: High-altitude hypoxia may exacerbate gastric mucosal damage by enhancing oxidative stress and inflammatory response induced by Hp infection. [ABSTRACT FROM AUTHOR]

Introduction: Cytokeratins (CKs) have been associated with precancerous and cancerous gastric lesions in patients with Helicobacter pylori-associated chronic gastritis, making them useful for diagnosing epithelial tumors. Methodology: A retrospective study was conducted utilizing 200 formalin-fixed paraffin-embedded gastric biopsy samples collected from the lesser curvature of the stomach. Samples from the control group, patients with H. pylori infection, and patients with H. pylori-associated gastritis, with complete and incomplete intestinal metaplasia (IM) were immunostained. Monoclonal antibodies were utilized to determine the expression of CK7, CK20, and Ki-67. Results: Patients infected with H. pylori had strong CK20 expression on the surface, and weak CK7 expression on the surface and deep glands; while non-specific chronic gastritis patients had weak focal CK7 expression and strong CK20 expression. The normal gastric mucosa of patients in the control group had relatively weak CK7 expression, restricted to a few cells in the neck and deep glands. CK20 showed diffuse strong reactivity on the surface. On the other hand, patients with complete IM showed a CK7 staining pattern that was either negative or weakly focal on the surface and crypts associated with diffuse surface CK20 and focal crypt staining corresponding to gastric type IM. The Ki67 proliferating index was low (≤ 15%) in H. pylori infected patients, high (> 30%) in patients with incomplete IM, and intermediate (16--30%) in patients with complete IM. Conclusions: These results indicate a significant link between the expressions of CK7/CK20 and Ki67 in patients afflicted with H. pylori and IM. [ABSTRACT FROM AUTHOR]

Background: The optimal duration of regimens for tailored therapy based on genotypic resistance for clarithromycin has yet to be established. Aim: This study was a nationwide, multicenter, randomized trial comparing empirical therapy with tailored therapy based on genotypic resistance for first‐line eradication of Helicobacter pylori. We also compared the eradication rates of 7‐ and 14‐day regimens for each group. Patients and Methods: Patients with H. pylori infection were first randomized to receive empirical or tailored therapy. Patients in each group were further randomized into 7‐ or 14‐day regimens. Empirical therapy consisted of a triple therapy (TT) regimen (twice‐daily doses of pantoprazole 40 mg, amoxicillin 1 g, and clarithromycin 500 mg) for 7 or 14 days. Tailored therapy consisted of TT of 7 or 14 days in patients without genotypic resistance. Patients with genotypic resistance were treated with bismuth quadruple therapy (BQT) regimens (twice‐daily doses of pantoprazole 40 mg, three daily doses of metronidazole 500 mg, and four times daily doses of bismuth 300 mg and tetracycline 500 mg) for 7 or 14 days. A 13C‐urea breath test assessed eradication rates. The primary outcome was eradication rates of each group. Results: A total of 593 patients were included in the study. The eradication rates were 65.7% (201/306) in the empirical therapy group and 81.9% (235/287) in the tailored therapy group for intention‐to‐treat analysis (p < 0.001). In the per‐protocol analysis, the eradication rates of the empirical therapy and tailored groups were 70.3% (201/286) and 85.5% (235/274) (p < 0.001), respectively. There was no difference in compliance between the two groups. The rate of adverse events was higher in the tailored group compared to the empirical group (p < 0.001). Discussion: Our study confirmed that tailored therapy based on genotypic resistance was more effective than empirical therapy for H. pylori eradication in Korea. However, no significant difference was found between 7‐ and 14‐day regimens for each group. Future studies are needed to determine the optimal duration of therapy for empirical and tailored therapy regimens. [ABSTRACT FROM AUTHOR]

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<0.05). MIR124-3 and TWIST1 methylation levels were higher in patients with IM than those with CG and also in those with GC than in those with IM (all q<0.05). A higher methylation level of TWIST1 was an independent predictor for H. pylori-negative GC after adjusting for age, sex, and atrophy (odds ratio [OR], 15.15; 95% confidence interval [CI], 1.58 to 145.46; p=0.018). The combination of TWIST1 methylation and GC microbiome index (a microbiome marker) was significantly associated with H. pylori-negative GC after adjusting for age, sex, and atrophy (OR, 50.00; 95% CI, 1.69 to 1,476; p=0.024). Conclusions: The combination of TWIST1 methylation and GC microbiome index may offer potential as a biomarker for predicting H. pylori-negative GC. ( [ABSTRACT FROM AUTHOR]

The Epstein-Barr viwrus (EBV) is a common herpesvirus that affects more than 90% of people worldwide. Even while EBV infections are frequently asymptomatic, they can cause autoimmune diseases and a number of cancers, especially in those with impaired immune systems. The intricate relationships between EBV and other coinfecting pathogens, including as human immunodeficiency virus (HIV), human papilloma virus (HPV), cytomegalovirus (CMV), and Plasmodium species, are examined in this study. We investigated the fundamental processes of these coinfections, their effects on the course of the disease, and their practical ramifications. The study reviewed how co-infections with EBV might modify immune responses, promote oncogenesis, and make treatment plans more challenging. In this review, we also discussed current therapeutic strategies, such as targeted molecular interventions, EBV vaccines, and adoptive T-cell therapy. The review underscores the need for more research to provide more focused and effective therapies that address the mutually reinforcing effects of numerous infections in disorders linked with EBV.

Background: Detecting Helicobacter pylori in fecal samples is easier and more comfortable than invasive techniques, especially in children. Thus, the objective of the present work was to detect H. pylori in feces from children by molecular methods as an alternative for diagnostic and epidemiological studies. Methods: Forty-five fecal samples were taken from pediatric patients who presented symptoms compatible with H. pylori infection. HpSA test, culture, real-time quantitative PCR (qPCR), fluorescence in situ hybridization (FISH), direct viable count associated with FISH (DVC-FISH), and Illumina-based deep-amplicon sequencing (DAS) were applied. Results: No H. pylori colonies were isolated from the samples. qPCR analysis detected H. pylori in the feces of 24.4% of the patients. In comparison, DVC-FISH analysis showed the presence of viable H. pylori cells in 53.3% of the samples, 37% of which carried 23S rRNA mutations that confer resistance to clarithromycin. After DAS, H. pylori-specific 16S rDNA sequences were detected in 26 samples. In addition, DNA from H. hepaticus was identified in 10 samples, and H. pullorum DNA was detected in one sample. Conclusion: The results of this study show the presence of H. pylori, H. hepaticus, and H. pullorum in children's stools, demonstrating the coexistence of more than one Helicobacter species in the same patient. The DVC-FISH method showed the presence of viable, potentially infective H. pylori cells in a high percentage of the children's stools. These results support the idea that fecal–oral transmission is probably a common route for H. pylori and suggest possible fecal–oral transmission of other pathogenic Helicobacter species. [ABSTRACT FROM AUTHOR]

Non-antibiotic adjuncts may improve Helicobacter pylori infection control. Our aim was to emphasize curcumin benefits in controlling H. pylori infection. We discussed publications in English mostly published since 2020 using keyword search. Curcumin is the main bioactive substance in turmeric. Curcumin inhibited H. pylori growth, urease activity, three cag genes, and biofilms through dose- and strain-dependent activities. Curcumin also displayed numerous anticancer activities such as apoptosis induction, anti-inflammatory and anti-angiogenic effects, caspase‐3 upregulation, Bax protein enhancement, p53 gene activation, and chemosensitization. Supplementing triple regimens, the agent increased H. pylori eradication success in three Iranian studies. Bioavailability was improved by liposomal preparations, lipid conjugates, electrospray-encapsulation, and nano-complexation with proteins. The agent was safe at doses of 0.5–>4 g daily, the most common (in 16% of the users) adverse effect being gastrointestinal upset. Notably, curcumin favorably influences the intestinal microbiota and inhibits Clostridioides difficile. Previous reports showed the inhibitory effect of curcumin on H pylori growth. Curcumin may become an additive in the therapy of H. pylori infection, an adjunct for gastric cancer control, and an agent beneficial to the intestinal microbiota. Further examination is necessary to determine its optimal dosage, synergy with antibiotics, supplementation to various eradication regimens, and prophylactic potential. [ABSTRACT FROM AUTHOR]

Gastric ulcer is a common disease affecting pigs worldwide, with a prevalence reported as high as 93%. The cause of porcine gastric ulcer is multifactorial, with Helicobacter suis (H. suis) being considered as the primary pathogenic factor. To date, prevalence of H. suis resulting in porcine gastric ulcer in Taiwan has not been investigated. In this study, we collected 360 pig stomachs from the slaughterhouses. In addition, stomach tissues from the 88 diseased pigs submitted for necropsy were divided into symptomatic and asymptomatic groups. Gastric lesions were scored, and polymerase chain reaction was used to determine the occurrence of gastric ulcer and the prevalence of H. suis. The positive rate of H. suis in the samples from slaughtered pigs was 49.7%, and both infection of H. suis and the presence of gastric lesions were prone to occur in autumn. The positive rates of H. suis infection in the symptomatic and asymptomatic groups were 59.1% and 31.8%, respectively. Moreover, the proportion of the samples with gastroesophageal ulcer in the symptomatic group was 68.2%, predominantly observed in growing pigs. The incidence of the samples from the slaughterhouses with gastroesophageal erosion to ulceration revealed a significant difference between H. suis -infected and H. suis -uninfected pigs; however, there is no significant difference in the samples of diseased pigs. In conclusion, H. suis infection was associated with gastric ulcer in slaughtered pigs, but it was not the primary cause of gastroesophageal ulcer in diseased pigs with clinical symptoms. [ABSTRACT FROM AUTHOR]

Aims: This study investigates the activity of the broad-spectrum bacteriocin nisin against a large panel of Gram-negative bacterial isolates, including relevant plant, animal, and human pathogens. The aim is to generate supportive evidence towards the use/inclusion of bacteriocin-based therapeutics and open avenues for their continued development. Methods and Results: Nisin inhibitory activity was screened against a panel of 575 strains of Gram-negative bacteria, encompassing 17 genera. Nisin inhibition was observed in 309 out of 575 strains, challenging the prevailing belief that nisin lacks effectiveness against Gram-negative bacteria. The genera Acinetobacter, Helicobacter, Erwinia, and Xanthomonas exhibited particularly high nisin sensitivity. Conclusions: The findings of this study highlight the promising potential of nisin as a therapeutic agent for several key Gram-negative plant, animal, and human pathogens. These results challenge the prevailing notion that nisin is less effective or ineffective against Gram-negative pathogens when compared to Gram-positive pathogens and support future pursuits of nisin as a complementary therapy to existing antibiotics. Significance and Impact of Study: This research supports further exploration of nisin as a promising therapeutic agent for numerous human, animal, and plant health applications, offering a complementary tool for infection control in the face of multidrug-resistant bacteria. [ABSTRACT FROM AUTHOR]

We have previously isolated a gram‐negative microaerophilic strain, PAGU2000T from a patient presenting with a fever in Kumamoto Prefecture, Japan. The present study aimed to comprehensively analyze the taxonomy of the isolated strain using a polyphasic approach. The 16S rRNA gene sequence analysis indicated that the strain was a member of enterohepatic Helicobacter. The strain PAGU2000T shared a 97.5% 16S rRNA gene nucleotide identity with Helicobacter valdiviensis, and this taxonomic position was confirmed by phylogenetic analysis of the GyrA amino acid sequences. The proposed strain PAGU2000T has a 1.482 Mbp chromosome with a DNA G + C content of 31.3 mol% and encodes 1520 predicted coding sequences. The average nucleotide identity between the strain PAGU2000T and type strain of H. valdiviensis was 70.3%, which was lower than the recommended threshold of 95% for species delineation. The strain PAGU2000T was a motile, non‐spore‐forming, and spiral‐shaped bacterium, exhibiting catalase and oxidase activities but not urease and nitrate reduction. This study demonstrates that the isolate represents a novel species within enterohepatic Helicobacter, for which the name Helicobacter higonensis is proposed (type strain: PAGU2000T = GTC 16811T = LMG 33095T). In this study, we describe the phenotypic and morphological features of this strain and propose an emended description of some biochemical traits of H. valdiviensis. [ABSTRACT FROM AUTHOR]

Background: At present, eradication regimens for non-Helicobacter pylori Helicobacter (NHPH) have not been established yet. We investigated effectiveness of the standard triple-drug combination therapy for Helicobacter pylori eradication and of a proton pump inhibitor (PPI) monotherapy in eradication of NHPH. Methods: Subjects were the patients who were diagnosed with NHPH-infected gastritis based on microscopic findings, helical-shaped organisms obviously larger than Helicobacter pylori, in the gastric mucosal specimens using Giemsa staining at Kenwakai Hospital between November 2010 and September 2021, whose NHPH species were identified by polymerase chain reaction (PCR) analysis of urease genes in endoscopically-biopsied samples, and who consented to NHPH eradication with either the triple-drug combination therapy for one week or a PPI monotherapy for six months. Six months after the completion of eradication, its result was determined with esophagogastroduodenoscopy, microscopic examination, and PCR analysis. In cases of unsuccessful eradication, a second eradication with the other therapy was suggested to the patient. Results: PCR analysis detected NHPH in 38 patients: 36 as Helicobacter suis and two as Helicobacter heilmannii/Helicobacter ailurogastricus. Fourteen Helicobacter suis-infected and one Helicobacter heilmannii/Helicobacter ailurogastricus-infected patients requested eradication therapy. The triple-drug combination therapy succeeded in four of five patients, while the PPI monotherapy succeeded in five of 10 patients. Three of five patients who had been unsuccessful with the latter therapy requested the triple-drug combination therapy as the second eradication and all three were successful. In total, the triple-drug combination therapy succeeded in seven out of eight (87.5%) attempted cases, while the PPI monotherapy in five out of 10 (50%) attempted cases. Conclusions: In NHPH eradication, the triple-drug combination therapy was considered to be effective to some extent and to become the first-line therapy. While, although less successful, PPI monotherapy appeared to be a potentially promising option particularly for patients with allergy or resistance to antibiotics. Effectiveness of PPI monotherapy may be attributed to hyperacid environment preference of Helicobacter suis and PPI's acid-suppressive effect. Additionally, male predominance in NHPH-infected gastritis patients may be explained by gender difference in gastric acid secretory capacity. However, further evidence needs to be accumulated. Study registration: This study was approved by the Research Ethics Committee of Kenwakai Hospital (No. 2,017,024). [ABSTRACT FROM AUTHOR]

Summary: Immune thrombocytopenia (ITP) is characterized by early platelet destruction and impaired platelet production. Helicobacter pylori (H. pylori) infection seems to contribute to the pathogenesis in certain ITP patients in Japan. We compared the effectiveness of platelet transfusion in severe ITP in the presence or absence of H. pylori. The median corrected count increment (CCI) at 24 h after platelet transfusion (CCI‐24) of the H. pylori‐positive ITP patients was higher than that of the H. pylori‐negative ITP patients (6463 vs. 754, p < 0.001), and the CCI‐1 was also in the same direction but not significant (23 351 vs. 11 578). Multiple regression analyses showed that H. pylori infection was independently associated with CCI‐24. Our study suggests that platelet transfusion may be more effective in H. pylori‐positive ITP patients. [ABSTRACT FROM AUTHOR]

Background: Helicobacter pylori (H. pylori) causes sterility by affecting the reproductive system. Vitamin B12 improves sperm quantity and function. Objective: Vitamin B12 protection against H. pylori adverse effects was investigated. Materials and Methods: 40 C57 male mice (6 wk) were randomly assigned to 4 equal groups (n = 10) including, group 1 (control without any intervention), group 2 (H), 3 (HP), and 4 (HB) received 1x109 colony forming unit (CFU) of H. pylori, 1x109 CFU of H. pylori+phosphate buffered saline, 1x109 CFU of H. pylori+50 μg/kg vitamin B12 intraperitoneally, respectively. In the induction groups, the H. pylori was orogasterically injected 3 times with 1 cc phosphate buffered saline throughout the day. Then testicular metrics, sperm motility, viability, quantity, and shape, plasma levels of malondialdehyde (MDA), superoxide dismutase, glutathione peroxidase, and total antioxidant capacity were measured. Also, testicular-tissue changes were examined using Johnson scores, tubular differentiation index, and spermatogenesis index. Vitamin B12, homocysteine, and testosterone serum levels were examined. Results: The results showed a significantly lower Johnson score, tubular differentiation index, and spermatogenesis index, and serum level of testosterone and homocysteine as well as a higher MDA level in the H and HP groups than the HB group (p < 0.05). In contrast, the highest superoxide dismutase and glutathione peroxidase enzymes activity and total antioxidant capacity as well as the lowest serum level of MDA were found in the HB group compared to other groups (p <0.05). Conclusion: Vitamin B12 increased antioxidant enzyme activity, enhanced sperm parameters, and decreased injury to testicular tissue. It can be used as a potent antioxidant in reducing testicular damage induced by H. pylori. [ABSTRACT FROM AUTHOR]

Background: The formation of gallstones is often accompanied by chronic inflammation, and the mechanisms underlying inflammation and stone formation are not fully understood. Our aim is to utilize single‐cell transcriptomics, bulk transcriptomics, and microbiome data to explore key pathogenic bacteria that may contribute to chronic inflammation and gallstone formation, as well as their associated mechanisms. Methods: scRNA‐seq data from a gallstone mouse model were extracted from the Gene Expression Omnibus (GEO) database and analyzed using the FindCluster() package for cell clustering analysis. Bulk transcriptomics data from patients with gallstone were also extracted from the GEO database, and intergroup functional differences were assessed using GO and KEGG enrichment analysis. Additionally, 16S rRNA sequencing was performed on gallbladder mucosal samples from asymptomatic patients with gallstone (n = 6) and liver transplant donor gallbladder mucosal samples (n = 6) to identify key bacteria associated with stone formation and chronic inflammation. Animal models were constructed to investigate the mechanisms by which these key pathogenic bacterial genera promote gallstone formation. Results: Analysis of scRNA‐seq data from the gallstone mouse model (GSE179524) revealed seven distinct cell clusters, with a significant increase in neutrophil numbers in the gallstone group. Analysis of bulk transcriptomics data from patients with gallstone (GSE202479) identified chronic inflammation in the gallbladder, potentially associated with dysbiosis of the gallbladder microbiota. 16S rRNA sequencing identified Helicobacter pylori as a key bacterium associated with gallbladder chronic inflammation and stone formation. Conclusions: Dysbiosis of the gallbladder mucosal microbiota is implicated in gallstone disease and leads to chronic inflammation. This study identified H. pylori as a potential key mucosal resident bacterium contributing to gallstone formation and discovered its key pathogenic factor CagA, which causes damage to the gallbladder mucosal barrier. These findings provide important clues for the prevention and treatment of gallstones. [ABSTRACT FROM AUTHOR]

Background: Educational initiatives on Helicobacter pylori (H. pylori) constitute a highly effective approach for preventing its infection and establishing standardized protocols for its eradication. ChatGPT, a large language model, is a potentially patient‐friendly online tool capable of providing health‐related knowledge. This study aims to assess the accuracy and repeatability of ChatGPT in responding to questions related to H. pylori. Materials and Methods: Twenty‐one common questions about H. pylori were collected and categorized into four domains: basic knowledge, diagnosis, treatment, and prevention. ChatGPT was utilized to individually answer the aforementioned 21 questions. Its responses were independently assessed by two experts on H. pylori. Questions with divergent ratings were resolved by a third reviewer. Cohen's kappa coefficient was calculated to assess the consistency between the scores of the two reviewers. Results: The responses of ChatGPT on H. pylori‐related questions were generally satisfactory, with 61.9% marked as "completely correct" and 33.33% as "correct but inadequate." The repeatability of the responses of ChatGPT to H. pylori‐related questions was 95.23%. Among the responses, those related to prevention (comprehensive: 75%) had the best response, followed by those on treatment (comprehensive: 66.7%), basic knowledge (comprehensive: 60%), and diagnosis (comprehensive: 50%). In the "treatment" domain, 16.6% of the ChatGPT responses were categorized as "mixed with correct or incorrect/outdated data." However, ChatGPT still lacks relevant knowledge regarding H. pylori resistance and the use of sensitive antibiotics. Conclusions: ChatGPT can provide correct answers to the majority of H. pylori‐related queries. It exhibited good reproducibility and delivered responses that were easily comprehensible to patients. Further enhancement of real‐time information updates and correction of inaccurate information will make ChatGPT an essential auxiliary tool for providing accurate H. pylori‐related health information to patients. [ABSTRACT FROM AUTHOR]

Background:Helicobacter pylori (H. pylori) infection is the most prevalent type of bacterial infection. Current guidelines from different regions of the world neglect specific African conditions and requirements. The African Helicobacter and Microbiota Study Group (AHMSG), founded in 2022, aimed to create an Africa-specific consensus report reflecting Africa-specific issues. Summary: Eighteen experts from nine African countries and two European delegates supported by nine African collaborators from eight other countries prepared statements on the most important African issues in four working groups: (1) epidemiology, (2) diagnosis, (3) indications and prevention, and (4) treatment. Limited resources, restricted access to medical systems, and underdeveloped diagnostic facilities differ from those of other regions. The results of the individual working groups were presented for the final consensus voting, which included all board members. Key Messages: There is a need for further studies on H. pylori prevalence in Africa, with diagnosis hinged on specific African situation. Treatment of H. pylori in the African setting should be based on accessibility and reimbursement, while indication and prevention should be defined in specific African countries. [ABSTRACT FROM AUTHOR]

Gastric cancer is considered a class 1 carcinogen that is closely linked to infection with Helicobacter pylori (H. pylori), which affects over 1 million people each year. However, the major challenge to fight against H. pylori and its associated gastric cancer due to drug resistance. This research gap had led our research team to investigate a potential drug candidate targeting the Helicobacter pylori‐carcinogenic TNF‐alpha‐inducing protein. In this study, a total of 45 daidzein derivatives were investigated and the best 10 molecules were comprehensively investigated using in silico approaches for drug development, namely pass prediction, quantum calculations, molecular docking, molecular dynamics simulations, Lipinski rule evaluation, and prediction of pharmacokinetics. The molecular docking study was performed to evaluate the binding affinity between the target protein and the ligands. In addition, the stability of ligand–protein complexes was investigated by molecular dynamics simulations. Various parameters were analysed, including root‐mean‐square deviation (RMSD), root‐mean‐square fluctuation (RMSF), radius of gyration (Rg), hydrogen bond analysis, principal component analysis (PCA) and dynamic cross‐correlation matrix (DCCM). The results has confirmed that the ligand–protein complex CID: 129661094 (07) and 129664277 (08) formed stable interactions with the target protein. It was also found that CID: 129661094 (07) has greater hydrogen bond occupancy and stability, while the ligand–protein complex CID 129664277 (08) has greater conformational flexibility. Principal component analysis revealed that the ligand–protein complex CID: 129661094 (07) is more compact and stable. Hydrogen bond analysis revealed favourable interactions with the reported amino acid residues. Overall, this study suggests that daidzein derivatives in particular show promise as potential inhibitors of H. pylori. [ABSTRACT FROM AUTHOR]

Helicobacter is a genus of spiral-shaped Gram-negative enterohepatic bacteria whose members are capable of causing bacteremia in humans. One of the poorly studied members of this genus is the bacterium Helicobacter cinaedi. This microorganism was first isolated from human fecal samples in 1984. Although it was long considered to be associated with only immunocompromised patients, more evidence in recent years has implicated H. cinaedi in causing serious pathologies in immunocompetent populations. In addition, H. cinaedi is also reported to be associated with a few chronic or severe illnesses, such as atherosclerosis, which in turn can lead to the development of other cardiovascular pathologies: one of the leading causes of mortality worldwide. Helicobacter cinaedi often goes unnoticed in standard diagnostic methods due to its slow growth under microaerobic conditions. This often leads to significant underdetection and hence undermines the role of this bacterium in the pathogenesis of various diseases and the extent of its spread in humans. In this review, we have compiled information on pathologies associated with H. cinaedi, the occurrence of the bacterium in humans and animals, and the latest developments in diagnosing the bacterium and treating associated diseases. [ABSTRACT FROM AUTHOR]

The involvement of Helicobacter-like agents in EGGD is not clear. Much evidence supports the presence of Helicobacter in the horse's stomach, but it is not so clear about the donkey. The present study was conducted to evaluate the presence of Helicobacter in the stomach of donkeys and assess the best method for its identification and its possible participation in EGGD and serum antioxidant status. Gastric juice sampling and biopsy from NMP and PA were performed by gastroscopic method from 12 donkeys. Histopathology and RUT were used to identify Helicobacter. TAC, THIOL, NO, and DPPH were measured to assess the antioxidant status of serum. Helicobacter was detected only by the RUT method in one donkey (8.33%), but it is unlikely that this infection was effective in causing EGGD. The RUT results for the three samples of gastric juice, NMP, and PA were not different. Histopathology of NMP and PA did not show Helicobacter infection. Helicobacter is present in the stomach of a donkey but does not change the antioxidant status of serum. The RUT is more efficient than H&E histopathology for the assessment of H. pylori in the equine stomach, and the RUT of gastric juice is preferable to tissue samples because it is easy, fast, and non-invasive. In conclusion, further studies using more accurate methods are recommended to evaluate the effect of Helicobacter in the gastric diseases of donkeys and other equine. [ABSTRACT FROM AUTHOR]

Helicobacter pylori infection is a well-established risk factor for the development of gastric cancer (GC). Understanding the immunopathogenesis underlying this association is crucial for developing effective preventive and therapeutic strategies. This narrative review comprehensively explores the immunopathogenesis of H. pylori-induced GC by delving into several key aspects, emphasizing the pivotal roles played by H. pylori virulence factors, including cytotoxin-associated gene A (cagA) and vacuolating cytotoxin A (vacA), blood group antigen-binding adhesin (babA), and sialic acid binding adhesin (sabA). Moreover, the review focuses on the role of toll-like receptors (TLRs) and cytokines in the complex interplay between chronic infection and gastric carcinogenesis. Finally, the study examines the association between H. pylori evasion of the innate and adaptive immune response and development of GC. A comprehensive understanding of the immunopathogenesis of H. pylori-induced GC is essential for designing targeted interventions to prevent and manage this disease. Further research is warranted to elucidate the intricate immune responses involved and identify potential therapeutic targets to improve patient outcomes.

The article discusses the potential of epigenetic markers and the gastric microbiome in predicting the risk of Helicobacter pylori-negative gastric cancer. While H. pylori infection is a well-established risk factor for gastric cancer, the risk remains even after eradication. The article suggests that analyzing aberrant DNA methylation in certain genes and studying the gastric microbiome may provide insights into the development of gastric cancer in H. pylori-negative patients. The study by Kim et al. examines the combined role of DNA methylation and the gastric microbiome in predicting H. pylori-negative gastric cancer, finding that higher methylation levels of certain genes and specific microbiome markers are associated with increased risk. Further research is needed to confirm these findings. [Extracted from the article]

Many bacteria and archaea rely on chemotaxis signal transduction systems for optimal fitness. These complex, multiprotein signaling systems have core components found in all chemotactic microbes, as well as variable proteins found in only some species. We do not yet understand why these variations exist or whether there are specific niches that favor particular chemotaxis signaling organization. One variation is in the presence/absence of the chemotaxis methylation adaptation enzymes CheB and CheR. Genes for CheB and CheR are missing in the gastric pathogen Helicobacter pylori but present in related Helicobacter that colonize the liver or intestine. In this work, we asked whether there was a general pattern of CheB/CheR across multiple Helicobacter species. Helicobacter spp. all possess chemotactic behavior, based on the presence of genes for core signaling proteins CheA, CheW, and chemoreceptors. Genes for the CheB and CheR proteins, in contrast, were variably present. Niche mapping supported the idea that these genes were present in enterohepatic Helicobacter species and absent in gastric ones. We then analyzed whether there were differences between gastric and enterohepatic species in the CheB/CheR chemoreceptor target methylation sites. Indeed, these sites were less conserved in gastric species that lack CheB/CheR. Lastly, we determined that cheB and cheR could serve as markers to indicate whether an unknown Helicobacter species was of enterohepatic or gastric origin. Overall, these findings suggest the interesting idea that methylation-based adaptation is not required in specific environments, particularly the stomach. IMPORTANCE Chemotaxis signal transduction systems are common in the archaeal and bacterial world, but not all systems contain the same components. The rationale for this system variation remains unknown. In this report, comparative genomics analysis showed that the presence/absence of CheR and CheB is one main variation within the Helicobacter genus, and it is strongly associated with the niche of Helicobacter species: gastric Helicobacter species, which infect animal stomachs, have lost their CheB and CheR, while enterohepatic Helicobacter species, which infect the liver and intestine, retain them. This study not only provides an example that a chemotaxis system variant is associated with particular niches but also proposes that CheB and CheR are new markers distinguishing gastric from enterohepatic Helicobacter species.

Helicobacter pullorum is an emerging foodborne pathogen that commonly colonizes the gastrointestinal tract of poultry, causing gastroenteritis. It has been related to several clinically important infections, including colitis and hepatitis, inflammatory bowel disease, recurrent diarrhea, and bacteremia in the human population. The bacterium may be transmitted to humans through undercooked poultry meat. In order to investigate the occurrence of H. pullorum in raw retail chicken meat (thighs and breasts), we analyzed 240 samples: 120 chicken thigh and 120 chicken breast samples. The samples were analyzed by means of an isolation protocol using Steele and McDermott's modified filtration technique on Brucella agar supplemented with 5% of defibrinated sheep's blood. The presumptive colonies were biochemically identified and analyzed using a previously described conventional PCR test based on the 16S rRNA gene. In total, 35% of analyzed samples were positive using the microbiological protocol and 45% were positive by PCR. These results suggest that H. pullorum can be transmitted to humans through the handling and consumption of raw poultry meat, representing a risk for food business operators and consumers. Efforts to control H. pullorum in broiler meat should prioritize the implementation of stringent hygienic practices across all stages of the food chain, from the farm to the consumer. [ABSTRACT FROM AUTHOR]

Background: Helicobacter pylori (H pylori) infection is the primary cause of gastric cancer (GC). The role of Disabled-2 (DAB2) in GC remains largely unclear. This study aimed to investigate the role of DAB2 in H pylori-mediated gastric tumorigenesis. Methods: We screened various datasets of GC to analyze DAB2 expression and cell signaling pathways. DAB2 expression was assessed in human GC tissue microarrays. H pylori infection in vivo and in vitro models were further explored. Immunostaining, immunofluorescence, chromatin immunoprecipitation, co-immunoprecipitation, Western blot, quantitative polymerase chain reaction, and luciferase reporter assays were performed in the current study. Results: The bioinformatic analysis verified that DAB2 was 1 of the 8 genes contributed to tumorigenesis and associated with poor prognosis in GC. The median overall survival and disease-free survival rates in DAB2high group were significantly less than those in DAB2low group. These findings demonstrated that H pylori transcriptionally activated DAB2 expression via signal transducer and activator of transcription 3 (STAT3)-dependent pathway. By bioinformatics analysis and knockdown or overexpression of DAB2, we found that DAB2 upregulated Yes-associated protein 1 (YAP1) transcriptional activity. Mechanistically, DAB2 served as a scaffold protein for integrin beta 3 (ITGB3) and SRC proto-oncogene non-receptor tyrosine kinase (SRC), facilitated the phosphorylation of SRC, promoted the small GTPase ras homolog family member A (RHOA) activation and phosphorylation of YAP1, and ultimately enhanced the YAP1 transcriptional activity. Conclusions: Altogether, these findings indicated that DAB2 is a key mediator in STAT3–regulated translation of YAP1 and plays crucial roles in H pylori-mediated GC development. DAB2 might serve as a novel therapeutic target for GC. [ABSTRACT FROM AUTHOR]

Background: The characteristic endoscopic findings of non‐Helicobacter pylori Helicobacter (NHPH) gastritis, including white marbled appearance and crack‐like mucosa, have been reported. However, these findings can also manifest in H. pylori (HP)‐infected gastritis. This study compared NHPH gastritis and mild atrophic HP gastritis to identify features that may enhance NHPH diagnosis. Materials and Methods: A total of 2087 patients underwent upper gastrointestinal endoscopy and were histologically evaluated by multiple gastric mucosal biopsies according to the updated Sydney System (USS) at Shinshu University Hospital between 2005 and 2023. Among them, nine patients were classified into the NHPH group and 134 patients with HP infection and mild atrophy were classified into the HP group for retrospective comparisons of endoscopic findings and clinicopathological characteristics. Results: All nine patients in the NHPH group (eight males [89%], median ± standard deviation [SD] age: 49 ± 13.0 years) were infected with H. suis. The 134 patients in the HP group contained 70 men (52%) and had a median ± SD age of 35 ± 19.9 years. Endoscopic findings were statistically comparable for white marbled appearance (three patients [33%] in the NHPH group and 37 patients [31%] in the HP group) and crack‐like mucosa (three patients [33%] and 27 patients [20%], respectively). Diffuse redness was significantly less frequent in the NHPH group (one patient [14%] vs. 97 patients [72%], p < 0.001). White marbled appearance or crack‐like mucosa without diffuse redness was significantly more common in the NHPH group (56% vs. 13%, p = 0.004), with a sensitivity and specificity of 56% and 87%, respectively. Mean USS neutrophil infiltration and Helicobacter density scores were significantly higher in the HP group (both p < 0.01), which might have influenced the endoscopic findings of diffuse redness. Conclusions: When endoscopic findings of white marbled appearance or cracked‐like mucosa are present, evaluation for diffuse redness may contribute to a more accurate diagnosis of NHPH gastritis. [ABSTRACT FROM AUTHOR]

Since the indications for endoscopic submucosal dissection have been expanded to include undifferentiated-type early gastric cancers, improvements in preoperative diagnostic ability have been an area of research. There are also concerns about the impact on the diagnosis of Helicobacter pylori infection. Based on our previous studies, in undifferentiated-type early gastric cancers, magnifying endoscopy with narrow-band imaging is useful for delineating the demarcation regardless of the tumor size. Additionally, inflammatory cell infiltration appears to be a cause of misdiagnosis, suggesting that the resolution of inflammation could contribute to the accurate diagnosis of demarcations. As such, the accuracy of demarcation in eradicated and uninfected cases is higher than that in non-eradicated cases. The common features of the endoscopic findings were discoloration under white-light imaging and a predominance of sites in the lower and middle regions. The uninfected group was characterized by smaller tumor size, flat type, more extended intervening parts in magnifying endoscopy with narrow-band imaging, and pure signet ring cell carcinoma. In contrast, the eradication and non-eradication groups were characterized by larger tumor size, depressed type, and wavy microvessels in magnifying endoscopy with narrow-band imaging. In this comprehensive review, as described above, we discuss the diagnosis of demarcation of undifferentiated-type early gastric cancers, undifferentiated-type early gastric cancers that developed following H. pylori eradication, and H. pylori-uninfected undifferentiatedtype early gastric cancers, with a focus on studies with self-examination and endoscopic findings and describe the future direction. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Laboratory Animal Science & Practices / Laboratuvar Hayvanlari Bilimi ve Uygulamalari Dergisi is the property of Ataturk University Coordinatorship of Scientific Journals 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.)

A total of 200 samples of chicken products collected randomly from Quesna and El-Bagour in Menoufia governorate. The collected samples were represented by chicken breast, thigh, gizzard and liver (50 of each) and subjected to bacteriological examination for detection of Helicobacter species particularly, Helicobacter pylori. Further, the effect of L. rhamnosus culture to control such serious pathogen contaminating chicken products was studied. Helicobacter spp., detected in 4%, 6%, 12% and 20% of breast, thigh, gizzard and liver, respectively and H. pylori represent 4%, 4% 6% and 10% from this examined samples, respectively. H. pylori inoculated chicken fillet (1×106/g) which are not treated with Lactobacillus rhamnosus (control +ve) showed increase in prevalence of H. pylori 1.0×106, 1.3×106, 1.9×106 and 2.4×106 at zero time, 1st day, 2nd day and 3rd day, respectively. While chicken fillets treated with L. rhamnosus (1x106/g) Effect on prevalence of H. pylori inoculated into chicken fillets with a reduction percent of 35%, 52% and 69% but L. rhamnosus (1x107/g) showed remarkable reduction of H. pylori prevalence with a reduction percent of 54%, 67% and 81% at 1st day, 2nd day and 3rd day, respectively. L. rhamnosus effected on virulence genes of H. pylori isolated from treated chicken fillet as L. rhamnosus (1x106/g) destructed cagA gene and L. rhamnosus (1x107/g) destructed cagA and vacA genes so using of Lactobacillus rhamnosus culture as a method of control has a good effect on prevalence of H. pylori and its virulence genes in chicken fillets and L. rhamnosus (1x107/g) more effective than L. rhamnosus (1x106/g). [ABSTRACT FROM AUTHOR]

Helicobacter pylori is one of the main predisposing factors for gastric cancer, causing chronic inflammation and proper glands atrophy in the gastric mucosa. Although H. pylori‐induced inflammation is a key inducer of precancerous lesions in the gastric mucosa, it remains unclear which precise immune cell subsets are responsible for the progression of H. pylori‐induced gastritis. Here, we observed an abundance of CD4+IL‐17A+FOXP3+ T cells exhibiting a Th17‐like phenotype within the microenvironment of H. pylori‐induced gastritis. Mechanistically, H. pylori upregulated the expression of IL‐6 in Dendritic cells and macrophages, by activating NF‐κB signaling through the virulence factor CagA and thus, induced IL‐17A expression in FOXP3+ T cells. Moreover, CD4+IL‐17A+FOXP3+ T cells were positively associated with advanced precancerous lesions. Therefore, these findings offer essential insights into how FOXP3+ T cells sense inflammatory signals from the environment, such as IL‐6, during H. pylori infections, thereby guiding the effector immune response and aggravating the gastritis. [ABSTRACT FROM AUTHOR]

Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphoma. The disease is very heterogeneous, with distinct genetic alterations in subtypes. The WHO 2022 5th edition classification identifies several minor groups of large B-cell lymphoma where the pathogenetic role of viruses (like EBV and HHV-8) is identified. Still, most cases fall into the group of DLBCL not otherwise specified (NOS). No review focuses only on this specific lymphoma type in the literature. The pathogenesis of this entity is still not fully understood, but several viruses and bacteria may have a role in the development of the disease. The authors review critical pathogenetic events in the development of DLBCL (NOS) and summarize the data available on several pathogenetic viruses and bacteria that have a proven or may have a potential role in the development of this lymphoma type. The possible role of B-cell receptor signaling in the microenvironment is also discussed. The causative role of the Epstein–Barr virus (EBV), human herpesvirus-8 (HHV-8), Hepatitis C virus (HCV), human immunodeficiency virus (HIV), Hepatitis B virus (HBV), and other viruses are explored. Bacterial infections, such as Helicobacter pylori, Campylobacter jejuni, Chlamydia psittaci, Borrelia burgdorferi, and other bacteria, are also reviewed. [ABSTRACT FROM AUTHOR]

This study investigated the role of causative infectious agents in ulceration of the non-glandular part of the porcine stomach (pars oesophagea). In total, 150 stomachs from slaughter pigs were included, 75 from pigs that received a meal feed, 75 from pigs that received an equivalent pelleted feed with a smaller particle size. The pars oesophagea was macroscopically examined after slaughter. (q)PCR assays for H. suis, F. gastrosuis and H. pylori-like organisms were performed, as well as 16S rRNA sequencing for pars oesophagea microbiome analyses. All 150 pig stomachs showed lesions. F. gastrosuis was detected in 115 cases (77%) and H. suis in 117 cases (78%), with 92 cases (61%) of co-infection; H. pylori-like organisms were detected in one case. Higher infectious loads of H. suis increased the odds of severe gastric lesions (OR = 1.14, p = 0.038), while the presence of H. suis infection in the pyloric gland zone increased the probability of pars oesophageal erosions [16.4% (95% CI 0.6–32.2%)]. The causal effect of H. suis was mediated by decreased pars oesophageal microbiome diversity [−1.9% (95% CI − 5.0–1.2%)], increased abundances of Veillonella and Campylobacter spp., and decreased abundances of Lactobacillus, Escherichia-Shigella, and Enterobacteriaceae spp. Higher infectious loads of F. gastrosuis in the pars oesophagea decreased the odds of severe gastric lesions (OR = 0.8, p = 0.0014). Feed pelleting had no significant impact on the prevalence of severe gastric lesions (OR = 1.72, p = 0.28). H. suis infections are a risk factor for ulceration of the porcine pars oesophagea, probably mediated through alterations in pars oesophageal microbiome diversity and composition. [ABSTRACT FROM AUTHOR]

Objectives: This study was performed to explore the preventive and therapeutic effects of Lactobacillus plantarum ZFM4 on H. pylori infections of the stomach tissue in C57BL/6 mice. Methods: In this study, 40 specific-pathogen-free female C57BL/6 mice were randomly divided into five groups, namely, the control, ZFM4 pretreatment) ZFM4 pretreatment before H. pylori infected), model (H. pylori infected), triple therapy (H. pylori infected and treated with triple therapy), and ZFM4 treatment groups (H. pylori infected and treated with ZFM4). The preventive and therapeutic effects of Lactobacillus plantarum ZFM4 were evaluated in H. pylori-infected C57BL/6 mice by assessing gastric tissue morphology, inflammatory cytokine levels, microbial composition, and microbial diversity. Results: Lactobacillus plantarum ZFM4 was able to survive in low gastric pH and play a role in preventing H. pylori infection. This was evident from a reduction in both, the gastric inflammatory response and expression of inflammatory factors caused by H. pylori infection. Lactobacillus plantarum ZFM4 could also inhibit the growth of H. pylori via its beneficial impact on the gastric microbiota. Conclusion: Our findings suggest that Lactobacillus plantarum ZFM4 offers superior preventive effects against H. pylori infections when used alone. However, the therapeutic effect on established infections is weaker. Further clinical trials are needed to confirm the specific dosage, duration, and other aspects of administration. [ABSTRACT FROM AUTHOR]

Purpose: Lower back pain (LBP), mainly caused by intervertebral disk (IVD) degeneration (IDD), is widely prevalent worldwide and is a serious socioeconomic burden. Numerous factors may trigger this degenerative process, and microbial dysbiosis has recently been implicated as one of the likely causes. However, the exact relationship between IDD and the microbiome remains obscure. In this study, we investigated the gut microbiota composition and fecal metabolic phenotype and discussed the possible influences of microbiome dysbiosis on IDD. Methods: Fecal DNA was extracted from 16 fecal samples (eight rabbit models with IDD and eight sex- and age-matched healthy controls) and analyzed by high-throughput 16S rDNA sequencing. The fecal samples were also analyzed by liquid chromatography–mass spectrometry-based metabolomics. Multivariate analyses were conducted for the relationship between the omics data and IDD, linear discriminant analysis effect size was employed for biomarker discovery. Moreover, the Kyoto Encyclopedia of Genes and Genomes (KEGG) database was used to annotate the differential metabolites. The potential correlation between differential gut microbiota and metabolites was then assessed. Results: The 16S rDNA sequencing results showed that the β-diversity of the gut microbiota was significantly different between the IDD and control groups, with distinct abundance levels of dominant genera. Moreover, 59 metabolites were significantly upregulated and 91 were downregulated in IDD rabbits versus the controls. The KEGG enrichment analysis revealed that the top pathways remarkably impacted by IDD were tyrosine metabolism, amino sugar and nucleotide sugar metabolism, benzoate degradation, ABC transporters, ascorbate and aldarate metabolism, pantothenate and CoA biosynthesis, and pyrimidine metabolism. The correlation analysis revealed that DL-tyrosine and N-acetylmuramic acid were associated with multiple differential bacterial genera, including Helicobacter and Vibrio, which may play important roles in the process of IVD degeneration. Conclusion: Our findings revealed that IDD altered gut microbiota and fecal metabolites in a rabbit model. The correlation analysis of microbiota and metabolome provides a deeper understanding of IDD and its possible etiopathogenesis. These results also provide a direction and theoretical basis for the clinical application of fecal transplantation, probiotics, and other methods to regulate gut microbiota in the treatment of LBP caused by IDD. [ABSTRACT FROM AUTHOR]

Background: The incidence of gastric neoplasms in Helicobacter pylori (Hp)-naïve patients has recently increased due to a remarkable decrease in the Hp-infected population in Japan. We investigated the clinicopathologic differences between Hp-infected gastric neoplasms (HpIGNs) and Hp-naïve gastric neoplasms (HpNGNs) that have not been fully elucidated so far. Methods: This retrospective multicenter study investigated 966 consecutive patients with 1131 gastric dysplasia or cancers who underwent endoscopic or surgical treatment for the recent decade. Clinicopathologic features were compared between HpIGN and HpNGN cases. Results: One thousand and sixty-eight HpIGNs in 916 patients included 877 differentiated types and 191 undifferentiated types. Sixty-three HpNGNs in 50 patients included 57 differentiated types (35 foveolar types, 15 intestinal types, 6 fundic-gland types, and 1 other differentiated type) and 6 undifferentiated types. HpNGNs occurred in younger (59.5 vs. 71.8 years, p < 0.05) and female patients (40.0% vs. 26.5%, p < 0.05), were found more frequently in the proximal compartment (p < 0.05), and had smaller size (median 4.0 vs. 20.0 mm, p < 0.05). Histologically, HpNGNs and HpIGNs both primarily consisted of differentiated type (90.5% vs. 82.1%, p = 0.089) and HpNGNs showed lower prevalence of invasive cancer (11.1% vs. 37.6%, p < 0.05) and lymphovascular invasion (1.6% vs. 31.6%, p < 0.05). Nearly all HpNGNs (62/63, 98.4%) were diagnosed in early pathological stage, while 16.1% (172/1068) of HpIGNs were diagnosed in advanced stage (p < 0.05). Conclusions: HpNGNs is recently on the increase but shows lower malignant nature regardless of histologic type than HpIGN. Endoscopic gastric cancer screening will be reviewed via cost effectiveness for Hp-naïve individuals in future. [ABSTRACT FROM AUTHOR]

Introduction: Extranodal marginal zone lymphoma (MZL) arises in a number of epithelial tissues, including the stomach, salivary gland, lung, small bowel, thyroid, ocular adnexa, skin, and elsewhere. It has also been called low-grade B-cell lymphoma of mucosa-associated lymphoid tissue (MALT). MALT lymphoma predominantly occurs in adults and is rare in children. Case Presentation: We report a case of MALT lymphoma involving the stomach, which is the most common subtype, in a 12-year-old girl. Initially, the patient relapsed after antibiotic therapy but achieved successful treatment subsequently through irradiation. Conclusion:Helicobacter pylori eradication therapy should be given to all patients with gastric MZL, irrespective of stage. In patients who do not respond to antibiotic therapy, treatment options such as irradiation and systemic cancer therapies should be considered, depending on the disease stage. [ABSTRACT FROM AUTHOR]

The site of enterohepatic Helicobacter colonization/infection in humans is still unknown. We report microbiologically and histopathologically confirmed H. fennelliae localization in the large intestine in an immunocompromised patient in Japan. This case contributes to better understanding of the life cycle of enterohepatic Helicobacter species. [ABSTRACT FROM AUTHOR]

Copyright of Revista Cientifica de la Facultade de Veterinaria is the property of Universidad del Zulia, Facultad de Ciencias Veterinarias 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.)

The cat gut-inhabitant conjoint microbiota is a peculiar ecosystem in relationship with several bodily functions and immunity. Gut microbiota dysbiosis could participate within autoimmune disease pathogenesis, whereas its niche, whether causative or influencing role regarding systemic immunity in autoimmune diseases, remains fugitive. The purpose of the present study was to identify gut microbiota alterations and probable mechanisms that participated in the development of Pemphigus foliaceus for a better understanding of future effective therapeutical armamentarium based on gut microbiota. In the present article, the authors investigated gut microbiota alterations to those of eight cats diagnosed with Pemphigus foliaceus. Furthermore, the study thoroughly analyzed pathogenic bacteria species as triggers of autoimmunity. The diagnostic algorithm involved two distinct sides: i) on referral with the first criteria was proof of evidence for possible autoimmunity, and ii) Pemphigus foliaceus diagnosis with relevant analytes. A total of eight cats were enrolled, and gut microbiomes were detected by the use of the MIDOG All-in-One Microbial Test targeting Next-Generation DNA Sequencing. By this methodology, we analyzed the dysbiosis network for bacterial kingdoms and determined the relationship between disease activity related to Pemphigus foliaceus and gut microbiota. The data showed increasing abundances of Collinsella, Lachnospiroceae, and Escherichia coli and decreasing Desulfovibrio piger, Prevotella copri, and Helicobacter cianedi among cats with pemphigus foliaceus. For the first time in Turkey, the gut microbiota of cats with pemphigus foliaceus were detected, the results of which could be cautiously taken into consideration for novel and effective therapeutical approaches. [ABSTRACT FROM AUTHOR]

The article discusses the transition of leadership in the scientific journal Helicobacter. Professor David Y. Graham, the founder and editor-in-chief of the journal, is stepping down after 28 years, and Professor Wai-Keung Leung will be taking over as the new editor. The article highlights Professor Graham's contributions to the field of Helicobacter research and the success of the journal under his leadership. It also emphasizes the ongoing importance of the journal in addressing unresolved issues related to Helicobacter and the potential for future research in the field. [Extracted from the article]

Yousry Esam-Eldin Abo-Amer,1 Amal Ahmed Mohamed,2 Mohamed Mahmoud Elhoseeny,3 Samar M Rezk,4 Sherief Abdel-Salam,5 Abdulmohsen H Alrohaimi,6 Asmaa Sayed Abdelgeliel,7 Seham Saeed Alzahrani,8 Ibrahim Jafri,8 Leena S Alqahtani,9 Eman Fayad,8 Mohamed Fakhry,10 Moataz Yousry Soliman11 1Mahala Hepatology Teaching Hospital, Hepatology& Gastroenterology Department, Gharbia, Elgharbia, Egypt; 2National Hepatology & Tropical Medicine Research Institute, Department of Biochemistry, Cairo, Egypt; 3Department of Internal Medicine, Faculty of Medicine, Suez University, Suez, Egypt; 4Department of Clinical Nutrition, Mahalla Hepatology Teaching Hospital, El-Mahalla El-Kubra, Elgharbia, Egypt; 5Department of Tropical Medicine, Hepatology & Gastroenterology Unit, Faculty of Medicine, Tanta University, Tanta, Egypt; 6Department of Pharmacy Practice, College of Pharmacy, Shaqra University, Shaqra, 11961, Saudi Arabia; 7Department of Botany & Microbiology, Faculty of Science, South Valley University, Qena, 83523, Egypt; 8Department of Biotechnology, College of Science, Taif University, Taif, 21944, Saudi Arabia; 9Department of Biochemistry, College of Science, University of Jeddah, Jeddah, 23445, Saudi Arabia; 10Department of Gastroenterology, Hepatology and Infectious Diseases, Faculty of Medicine, Al-Azhar University, Asyut, Egypt; 11Department of Hepatology, Gastroenterology and Infectious Diseases, Faculty of Medicine, Al-Azhar University, Cairo, EgyptCorrespondence: Sherief Abdel-Salam, Department of Tropical Medicine, Hepatology & Gastroenterology Unit, Faculty of Medicine, Tanta University, El-Bahr Street, Tanta, Egypt, Tel +201147773440, Email sheriefabdelsalam@yahoo.comBackground & Aims: This research aimed to determine how variations in the vitamin D receptor gene affected the response of H. pylori infections to eradication therapy.Patients and Methods: On 105 adult H. Pylori-positive patients, a prospective cohort study was carried out. PCR was used to genotype all patients’ VDR gene polymorphisms. The patients in the study received standard triple eradication medication (clarithromycin 500 mg, amoxicillin 1000 mg, and omeprazole 20 mg) twice daily for 14 days. A stool test for H. pylori Ag was conducted 4 weeks following the end of treatment.Results: In our study, the usual triple therapy’s H. pylori eradication rate was 75.2%. The successful eradication of H. pylori and VDR rs 2228570 gene polymorphisms was more prevalent in CT gene polymorphism (64.6%) compared to non-responders (19.2%), while treatment failure was more prevalent in CC gene polymorphism (73.1% in non-responders compared to responders 24.1%), which is statistically significant. In regards to the eradication of H. pylori and VDR rs7975232 gene polymorphisms, the success of eradication was more prevalent in AC gene polymorphism (54.4%) vs non-responders (30.4%), while all patients (14) with gene AA (17.7%) are responders to standard treatment, while the failure of treatment was more prevalent in CC gene polymorphism (69.2% in non-responder vs 27.8% in responders) which is statistically significant. Our findings demonstrated a strong correlation between patients’ responses to H. pylori treatment and polymorphisms in the VDR gene (ApaI and TaqI) (P 0.05).Conclusion: As far as we are aware, this is the first study to identify a potential link between the FokI and Apal VDR polymorphism and treatment response in H pylori-positive patients. To evaluate the findings, more research with larger number of patients and different population is required.Keywords: Helicobacter, infection, gene, polymorphism, response, eradication

In order to determine the presence of Helicobacter in shelter Dogs in Yozgat Province of Türkiye by fecal antigen test and ELISA and to treat the infection during the initial period. As the material of the study, faecal antigen test, faecal samples for ELISA, blood samples for haematological and biochemical analyses were collected from 82 dogs in Sorgun animal shelter where food and water bowls were kept in compartments. Infected and control groups were formed according to the results of the fecal antigen test. As a result of fecal antigen test, 6 of 82 animals were antigen positive and 76 were antigen negative. According to ELISA analysis; 53 dogs were antibody positive and 29 dogs were antibody negative. No significance was determined between the groups in terms of age and gender in both tests (P>0.05). Dogs in the infected group were treated according to a protocol known as triple therapy, which is used in Helicobacter infections. WBC, NEU and MON counts, RDW and % NEU values of the infected group were higher in the hematological examination, while the % LYM values were significantly lower than the control group. In the biochemical examination, the concentrations TNF–α (21.17 pg·mL-1 vs. 48.21 pg·mL-1), IL–1β (73.41 pg·mL-1 vs. 37.60 pg·mL-1) (P

Background: Fibroblasts, especially cancer-associated fibroblasts (CAFs), represent the predominant stromal cell population in the tumor microenvironment and have an important function in tumorigenesis by interacting with tumor cells. However, their interaction remains elusive in an inflammatory tumor microenvironment induced by Helicobacter pylori (H. pylori). Methods: The expression of Serpin family E member 1 (Serpin E1) was measured in fibroblasts with or without H. pylori infection, and primary gastric cancer (GC) cells. Serpin E1 knockdown and overexpression fibroblasts were generated using Serpin E1 siRNA or lentivirus carrying Serpin E1. Co-culture models of fibroblasts and GC cells or human umbilical vein endothelial cells (HUVECs) were established with direct contact or the Transwell system. In vitro functional experiments and in vivo tumorigenesis assay were employed to study the malignant behaviors of GC cells interacting with fibroblasts. ELISA was used for quantifying the levels of Serpin E1 and VEGFA in the culture supernatant. The tube formation capacity of HUVECs was assessed using a tube formation assay. Recombinant human Serpin E1 (recSerpin E1), anti-Serpin E1 antibody, and a MAPK pathway inhibitor were utilized to treat HUVECs for elucidating the underlying molecular mechanisms. Results: Serpin E1 was predominantly expressed in gastric CAFs. H. pylori infection significantly enhanced the expression and secretion of Serpin E1 by CAFs. Both fibroblast-derived Serpin E1 and recSerpin E1 enhanced the growth, invasion, and migration of GC cells, along with increased VEGFA expression and tube formation in HUVECs. Furthermore, the co-inoculation of GC cells and fibroblasts overexpressing Serpin E1 triggered the expression of Serpin E1 in cancer cells, which facilitated together xenograft tumor growth and peritoneal dissemination of GC cells in nude mice, with an increased expression of Ki67, Serpin E1, CD31 and/or VEGFA. These processes may be mediated by Serpin E1-induced migration and p38 MAPK/VEGFA-mediated angiogenesis of HUVECs. Conclusion: H. pylori infection induces Serpin E1 expression in fibroblasts, subsequently triggering its expression in GC cells through their interaction. Serpin E1 derived from these cells promotes the migration and p38 MAPK/VEGFA-mediated angiogenesis of HUVECs, thereby facilitating GC growth and peritoneal metastasis. Targeting Serpin E1 signaling is a potential therapy strategy for H. pylori-induced GC. [ABSTRACT FROM AUTHOR]

Objectives Gastric mucosa-associated lymphoid tissue (MALT) lymphoma is historically associated with Helicobacter pylori (HP) infections in more than 80% of patients. However, the incidence of HP-negative MALT lymphoma has been increasing. The clinicopathologic features have not been well studied, and optimal management strategies remain unclear. Methods The pathology database was searched for primary gastric MALT lymphomas diagnosed from 2000 to 2017. The clinical data and the slides were reviewed. The cases were divided for analysis into those with a background of chronic gastritis with HP, chronic gastritis without HP, and without either a background of chronic gastritis or HP. Results Of 70 gastric MALT lymphoma cases identified, 26 (37% of total) had chronic gastritis and were positive for HP histologically (n = 23) or were HP positive by additional laboratory testing (n = 3). The remaining 44 (63% of total) cases were HP negative by histology. Within the HP-negative cases, 5 (11% of HP-negative cases) showed histologic gastritis while 39 (89% of HP-negative cases) did not have sufficient evidence of gastritis through review of slides (n = 18) or based on available pathology reports (n = 21). The HP-negative cases without gastritis had higher propensities to show a mass lesion on endoscopy compared with HP-positive cases (37.5% vs 11.1%, P =.02) at the initial diagnosis. The immunophenotype and rate of positive B-cell gene rearrangement were not significantly different between the 2 groups. While all HP-positive patients received antibiotics for HP eradication, treatment in the HP-negative group varied among antibiotics, radiation, rituximab, or chemotherapy. Among HP-negative patients with available follow-up, 13 (39%) showed disease recurrence, similar to the recurrence rate in HP-positive patients; however, no individual from either group has died of the disease thus far. Conclusions The incidence of HP-negative MALT lymphoma is increasing, and in our practice, it is currently more common than HP-associated MALT lymphomas. The pathophysiology of HP-negative MALT lymphoma without chronic gastritis remains unclear. Follow-up data in our study suggest that the prognosis of these cases is excellent despite varied management modalities. [ABSTRACT FROM AUTHOR]