Correlation between Bacteria and Helicobacter Pylori Infection with Gastric Mucosal Diseases

Abstract

Objective: To explore the impact of the gastric microbiota in the development of gastric mucosal lesions. Methods: Forty-one gastric antrum and corpus mucosal samples were collected from patients with gastritis or peptic ulcer, and were divided into chronic superficial gastritis (CSG, n = 21), chronic atrophic gastritis (CAG, n = 12) and peptic ulcer (PU, n = 8) groups. 16S rRNA gene amplicons were sequenced by Pacific Biosciences Single Molecule Real Time (Pacbio SMRT) sequencing technology. QIIME (Quantitative Insights Into Microbial Ecology) software was used to calculate the α diversity metrics. Principal coordinate analysis (PCoA) was used to detect unweighted and weighted UniFrac distance. Linear discriminant effect size (LEfSe) analysis was used to assess the abundance of strains among groups. Results: The α diversity of the gastric microbiota in PU group decreased compared to CSG and CAG groups. Abundance of Helicobacter pylori (HP) in PU group was increased (82.3%), while the abundance of Lactobacillus was decreased compared to CSG and CAG group. Microbial community structure in PU group was separated from CAG and CSG groups (p = 0.015 and 0.001). Microbial community structure in HP positive samples was separated from HP negative samples in CSG and CAG groups. Overall, 41 strains with different abundance were found and identified in the CSG, CAG and PU groups. The enrichment of Proteobacteria, Helicobacter and HP were observed in the PU group. Conclusions: Gastric mucosal lesions severity reduced the diversity of the gastric microbiota, and increased the abundance of HP.