AUTHOR=Hua Zhaolai , Xu Le , Zhu Jiahui , Xiao Ling , Lu Bin , Wu Jianping , Wu Zhenfeng , Zhou Qihai , Zhang Junfeng 

TITLE=Helicobacter pylori infection altered gastric microbiota in patients with chronic gastritis

JOURNAL=Frontiers in Cellular and Infection Microbiology

VOLUME=13

YEAR=2023

URL=https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2023.1221433

DOI=10.3389/fcimb.2023.1221433

ISSN=2235-2988

ABSTRACT=<sec><title>Objective</title><p>The present study aims to investigate the effect of <italic>Helicobacter pylori</italic> (Hp) infection on gastric mucosal microbiota in patients with chronic gastritis.</p></sec><sec><title>Methods</title><p>Here recruited a population of 193 patients with both chronic gastritis and positive rapid urease, including 124 patients with chronic atrophic gastritis (CAG) and 69 patients with chronic non-atrophic gastritis (nCAG). Immunoblotting was used to detect four serum Hp antibodies (UreA, UreB, VacA and CagA) to determine the types of virulent Hp-I and avirulent Hp-II infections. Gastric microbiota was profiled by 16S rRNA gene V3-V4 region, and R software was used to present the relationship between the microbial characteristics and the type of Hp infection.</p></sec><sec><title>Results</title><p>In the stomach of patients with Hp-positive gastritis, the dominant gastric bacterial genera included <italic>Ralstonia</italic> (23.94%), <italic>Helicobacter</italic> (20.28%), <italic>Pseudonocardia</italic> (9.99%), <italic>Mesorhizobium</italic> (9.21%), <italic>Bradyrhizobium</italic> (5.05%), and <italic>Labrys</italic> (4.75%). The proportion of Hp-I infection was significantly higher in CAG patients (91.1%) than in nCAG patients (71.0%) (<italic>P</italic> &lt; 0.001). The gastric microbiota richness index (observed OTUs, Chao) was significantly lower in CAG patients than in nCAG patients (<italic>P &lt;</italic>0.05). Compared with avirulent Hp-II infection, virulent Hp-I infection significantly decreased the Shannon index in CAG patients (<italic>P &lt;</italic>0.05). In nCAG patients, Hp-I infected patients had lower abundances of several dominant gastric bacteria (<italic>Aliidiomarina</italic>, <italic>Reyranella</italic>, <italic>Halomonas</italic>, <italic>Pseudomonas</italic>, <italic>Acidovorax</italic>) than Hp-II infected patients. Meanwhile, in CAG patients, Hp-I infected patients occupied lower abundances of several dominant oral bacteria (<italic>Neisseria</italic>, <italic>Staphylococcus</italic> and <italic>Haemophilus</italic>) than Hp-II infected patients. In addition, bile reflux significantly promoted the colonization of dominant oral microbiota (<italic>Veillonella</italic>, <italic>Prevotella 7</italic> and <italic>Rothia</italic>) in the stomach of CAG patients. There was no significant symbiotic relationship between <italic>Helicobacter</italic> bacteria and non-<italic>Helicobacter</italic> bacteria in the stomach of nCAG patients, while <italic>Helicobacter</italic> bacteria distinctly linked with the non-<italic>Helicobacter</italic> bacteria (<italic>Pseudolabrys</italic>, <italic>Ralstonia</italic>, <italic>Bradyrhizobium</italic>, <italic>Mesorhizobium</italic> and <italic>Variovorax</italic>) in CAG patients.</p></sec><sec><title>Conclusions</title><p>Virulent Hp infection alters the gastric microbiota, reduces microbial diversity, and enhances the symbiotic relationship between the <italic>Helicobacter</italic> bacteria and non-<italic>Helicobacter</italic> bacteria in patients with chronic gastritis. The data provides new evidence for treating Hp infection by improving the gastric microbiota.</p></sec>