The Effects of Helicobacter pylori Infection on Gastric Microbiota in Children With Duodenal Ulcer

Abstract

BackgroundHelicobacter 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.MethodsWe 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).ResultsBacterial 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.ConclusionsThe 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].

Integrating microbiome and metabolome revealed microbe-metabolism interactions in the stomach of patients with different severity of peptic ulcer disease

“…But interestingly, when our study analyzed the reclassification of the sample into H group (i.e., the original HC group) and D group (i.e., the original ME and PUD groups), this later analysis found that Helicobacter was not the differential genus ( Figure S4 ), suggesting to us that Helicobacter may be a characteristic flora of PUD patients while not being significant in HC and ME patients. Furthermore, Helicobacter had been shown to reduce the bacterial richness and diversity of the gastric flora ( 56 ), which was consistent with our findings. Relevant studies have reported the characteristics of Helicobacter ’s physiological metabolism, including glucose metabolism, bile acid metabolism, the respiratory chain (energy metabolism), amino acid metabolism, and other pathways ( 57 – 59 ).…”

“…In the present study, we found a profile of changes in the differential distribution of gastric flora in patients with PUD with different pathological processes. The abundance and diversity of microorganisms in the stomach decreased significantly during the development and progression of PUD, and a clinical study found that patients with chronic gastritis had a significantly higher alpha diversity index than patients with duodenal ulcers (35), which was consistent with our findings. Another clinical cohort study found that the microbiota of gastric cancer patients had lower microbial diversity than patients with chronic gastritis (36).…”

The Disease with a Thousand Faces and the Human Microbiome—A Physiopathogenic Intercorrelation in Pediatric Practice

“…With reference to the stomach, the main lines of research regarding bacterial colonization include its modification in Helicobacter pylori (H. pylori) infection, but also in chronic gastritis, duodenal ulcer or carcinogenesis, conditions in which the microbiota has been shown to have an altered diversity compared to the batches of control subjects, with part of its components showing causal relationships with the incriminated pathologies (e.g., Bacteroides-H. pylori in children or Methylobacterium in gastric carcinogenesis, being also a negative prognostic marker) [68][69][70]. About the influence of H. pylori and gastric dysbiosis among duodenal ulcer patients, Zheng W. et al postulated that in this situation, the character of infected/uninfected has the potential to modulate the community of genotoxic bacteria present at the level of the microbiota [71]. A role in this process seems to be played by iron, a constituent that, when found in low quantities, imprints the carcinogenic potential of H. pylori, possibly through the interaction with the metabolism of bile acids (especially deoxycholic acid) [72].…”

Gastrointestinal contrast-enhanced ultrasonography for diagnosis and treatment of peptic ulcer in children

“…Overseas studies have also shown that H. pylori is the main cause of peptic ulcer, and > 75% of duodenal ulcers and > 17% of gastric ulcers are associated with this infection[ 7 ]. In children with H. pylori -infected duodenal ulcers, the mucosal microbiota of the duodenal bulb is altered, characterized by an increased abundance of H. pylori and decreased abundance of Clostridium and Streptococcus , which possibly alters the biological function of the commensal microbiota through specific metabolic pathways[ 8 ]. A systematic review and meta-analysis that assessed the global prevalence of H. pylori infection found that more than half the population is infected[ 9 ].…”