# Helicobacter pylori causes gastric dysbacteriosis in chronic gastritis patients

## TL;DR

This study shows that Helicobacter pylori infection disrupts the stomach's bacterial balance in chronic gastritis patients, leading to inflammation and other harmful effects.

## Contribution

The study demonstrates how H. pylori causes gastric dysbacteriosis and validates these findings through animal experiments.

## Key findings

- H. pylori infection leads to significant changes in the composition of gastric flora in chronic gastritis patients.
- Infected mice showed increased inflammation, acid secretion, and oxidative stress compared to uninfected mice.
- Seven key metabolic pathways were altered in H. pylori-positive patients compared to H. pylori-negative individuals.

## Abstract

Gastric mucosal samples were procured and underwent the sequencing of 16S ribosomal RNA (16S rRNA) via Illumina high-throughput sequencing technology to explore the impact of Helicobacter pylori (H. pylori) infection on the composition of gastric flora in chronic gastritis (CG) patients. In the results, the operational taxonomic unit (OTU) analysis revealed an overlap of 5706 OTUs shared between the two groups. The top 5 abundance ranking (TOP5) phyla comprised Bacteroidetes, Proteobacteria, Firmicutes, Actinobacteria, and Epsilonbacteraeota, while the TOP5 genus was Lachnospiraceae_NK4A136_group, Helicobacter, Bacteroides, Klebsiella, and Pseudomonas. In the metabolic pathways at the Kyoto Encyclopedia of Genes and Genomes (KEGG)_L3 level, conspicuous variations across seven functions were observed between the H. pylori-positive (HP_Pos) and H. pylori-negative (HP_Neg) groups. Subsequently, functional gene enrichment in KEGG pathways was further validated through animal experimentation. In contrast to the mice in the HP_Neg group, those infected with H. pylori manifested an infiltration of inflammatory cells, an augmentation in gastric acid secretion, and conspicuously elevated scores regarding gastric activity, along with heightened levels of malondialdehyde. In conclusion, CG patients infected with H. pylori displayed a disorder in gastric flora, furnishing a theoretical basis for the prophylaxis of H. pylori infection and its associated pathogenic ramifications.