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Background: Helicobacter pylori (H. pylori) infection is the main cause of chronic gastritis and duodenal ulcer in children. Little is known about the effect of H. pylori on gastric microbiota in children with duodenal ulcer. This study is aimed at the characteristics of gastric microbiota in children with duodenal ulcer on H. pylori infection. Methods: We studied 23 children diagnosed with duodenal ulcer by gastric endoscopy because of the gastrointestinal symptoms, 15 children were diagnosed with H. pylori infection, while 8 children were without H. pylori infection. Endoscopic mucosal biopsy samples were obtained for DNA extraction. Microbiomes were analyzed by 16S rRNA profiling and microbial functions were predicted using the software Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt). Results: Bacterial richness and diversity of gastric microbiota in duodenal ulcer with H. pylori -positive were lower than those negative. The gastric microbiota in H. pylori -positive group significantly reduced proportions of six phyla and fifteen genera; only Helicobacter taxa were more abundant in H. pylori- positive group. Co-expression network analysis showed a more complex network of interactions in the H. pylori- positive group than that in the H. pylori- negative group. For the predicted functions, lower abundance in the pathways of carbohydrate metabolism, signal transduction, amino acid metabolism, and lipid metabolism were found in H. pylori- positive group than the H. pylori- negative group. H. pylori colonization reduces a microbial community with genotoxic potential in the gastric mucosa of children with duodenal ulcer. Conclusions: The presence of H. pylori significantly influences gastric microbiota and results in a lower abundance of multiple taxonomic levels in children with duodenal ulcer. Children with duodenal ulcer exhibit a dysbiotic microbial community with genotoxic potential, which is distinct from that of children with H. pylori infection. Clinical Trial Registration: [http://www.chictr.org.cn], identifier [ChiCTR1800015190]. [ABSTRACT FROM AUTHOR]

Background: Helicobacter pylori infection is the main cause of chronic gastritis in children. Little is known about the effect of Helicobacter pylori on microbiota and immunity. This study was aimed at characterizing stomach microbiota and immune-regulatory properties of children with Helicobacter pylori colonization. Methods: We studied 122 children who had undergone gastric endoscopy due to gastrointestinal symptoms, 57 were diagnosed with Helicobacter pylori infection. Endoscopic mucosal biopsy samples were obtained for DNA and RNA extraction. Microbiomes were analyzed by 16S rRNA profiling, with the differentially expressed genes analyzed using RNA sequencing. The RNA-sequencing results of selected genes were validated by qRT-PCR. Results: Bacterial diversity of Helicobacter pylori -positive gastric specimens were lower than those of negative, and both groups were clearly separated according to beta diversity. Helicobacter pylori -positive group significantly reduced proportions of six phyla and eight genera; only Helicobacter taxa were more abundant in Helicobacter pylori- negative group. Gastric tissues RNA sequencing showed increased expression of multiple immune response genes in Helicobacter pylori -infection. Helicobacter pylori -infected children with restructured gastric microbiota had higher levels of FOXP3, IL-10, TGF-β1 and IL-17A expressions, which were consistent with increased CD4+T cell and macrophagocyte, compared with non-infected children. Conclusions: Presence of Helicobacter pylori significantly influences gastric microbiota and results in lower abundance of multiple taxonomic levels in children. Meanwhile, it affects gastric immune environment and promotes the occurrence of gastritis. Clinical Trial Registration: [ http://www.chictr.org.cn ], identifier [ChiCTR1800015190] [ABSTRACT FROM AUTHOR]

Background and Aims: Helicobacter pylori (HP) culture for diagnosing HP infection is time‐consuming and technologically complex. This study evaluated the clinical significance of gastric mucosal gene chip technology in the rapid diagnosis of HP infection and detection of drug resistance in children. Methods: Patients (between the age of 2.5 and 16.0 years old) manifesting gastrointestinal symptoms were enrolled in this study. HP culture of gastric mucosa and drug sensitivity test were performed. A gene chip of gastric mucosa was used to detect the presence of HP infection, some single nucleotide polymorphisms in HP drug resistance genes, or associated gene mutation. DNA sequencing was investigated and compared with the gene chip test results. Results: Out of 267 cases, HP culture was positive in 169 cases and negative in 98 cases. HP detection by the gene chip method was positive in 208 cases and negative in 59 cases. The sensitivity, specificity, and accuracy of the gene chip technology for diagnosing HP infection were 96.1, 85.0, and 93.6%, respectively. HP resistance gene locus using the gene chip showed the main mutation locus of clarithromycin to be 2143A/G, levofloxacin at locus GyrA 91 and GyrA 87, and amoxicillin at PBP1 556ser. Concordance rates between gene chip and DNA sequencing for VacA‐S/M, 16S rRNA, 23S rRNA, and GyrA were greater than 95%, and that of PBP1 was greater than 82%. Conclusion: Gastric mucosal gene chip technology can be used for rapid diagnosis and drug resistance detection of HP infection in children. [ABSTRACT FROM AUTHOR]

Abstract: Background: The decreasing eradication rate of Helicobacter pylori is mainly because of the progressive increase in its resistance to antibiotics. Studies on antimicrobial susceptibility of H. pylori in children are limited. This study aimed to investigate the resistance rates and patterns of H. pylori strains isolated from children. Materials and Methods: Gastric mucosa biopsy samples obtained from children who had undergone upper gastrointestinal endoscopy were cultured for H. pylori, and susceptibility to six antibiotics (clarithromycin, amoxicillin, gentamicin, furazolidone, metronidazole, and levofloxacin) was tested from 2012‐2014. Results: A total of 545 H. pylori strains were isolated from 1390 children recruited. The total resistance rates of H. pylori to clarithromycin, metronidazole, and levofloxacin were 20.6%, 68.8%, and 9.0%, respectively. No resistance to amoxicillin, gentamicin, and furazolidone was detected. 56.1% strains were single resistance, 19.6% were resistant to more than one antibiotic, 16.7% for double resistance, and 2.9% for triple resistance in 413 strains against any antibiotic. And the H. pylori resistance rate increased significantly from 2012‐2014. There was no significant difference in the resistance rates to clarithromycin, metronidazole, and levofloxacin between different gender, age groups, and patients with peptic ulcer diseases or nonulcer diseases. Conclusions: Antibiotic resistance was indicated in H. pylori strains isolated from children in Hangzhou, and it increased significantly during the 3 years. Our data strongly support current guidelines, which recommend antibiotic susceptibility tests prior to eradication therapy. [ABSTRACT FROM AUTHOR]

Nodular gastritis (NG) represents a frequently observed clinical presentation of Helicobacter pylori (H. pylori) infection in pediatric patients. This investigation aimed to explore the microbiota and histological features of the gastric mucosa in children with H. pylori colonized NG. The current investigation examined a sample of 120 children who underwent gastroscopy due to symptoms of gastrointestinal distress, which showed that 64 were patients with H. pylori infection. Endoscopic procedures were conducted to acquire mucosal biopsies for the purpose of DNA extraction and histopathological analysis. The 16S rRNA profiling was utilized to examine the gastric mucosal microbiota. In conjunction with endoscopic evaluation, 26 of 64 patients were diagnosed with NG. The NG group had significantly higher inflammation scores and activity scores on histological assessment than the non-NG group. The NG group exhibited a significant reduction in the richness levels of the five genera. In terms of the predicted functions, the pathways of synthesis and degradation of ketone bodies and phagosome in the NG group were less abundant compared with the non-NG group, while the Wnt signaling pathway was significantly enriched. NG does not increase a microbial community that possesses genotoxic potential within the gastric mucosa. In conclusion, NG group exhibited significant severe inflammation and reduced abundance levels of several bacterial genera compared to the non-NG group. However, individuals with NG did not have a dysregulated microbial community with genotoxic potential. • Nodular gastritis (NG) group had significantly higher inflammation scores and activity scores on histological assessment than the non-NG group. • There was a degree of difference between the two groups in terms of population abundance levels, co-network analysis and functional prediction. • NG does not increase a microbial community that possesses genotoxic potential within the gastric mucosa, suggesting that children with nodular gastritis do not have an increased risk of mucosal carcinogenesis. [ABSTRACT FROM AUTHOR]