Abstract
Helicobacter pylori infection changes gastric microbiota profiles. However, it is not clear whether H. pylori eradication can restore the healthy gastric microbiota. Moreover, there has been no study regarding the changes in gastric microbiota with aging. The objective of this study was to investigate the changes in gastric corpus microbiota with age and following H. pylori eradication. Changes in corpus mucosa-associated microbiota were evaluated in 43 individuals with endoscopic follow-up > 1 year, including 8 H. pylori-uninfected and 15 H. pylori-infected subjects with no atrophy/metaplasia by histology and pepsinogen I/II ratio > 4.0; 17 H. pylori-infected subjects with atrophy/metaplasia and pepsinogen I/II ratio < 2.5; and 3 subjects with atrophy/metaplasia, no evidence of active H. pylori infection, negative for anti-H. pylori immunoglobulin G (IgG) antibody testing, and no previous history of H. pylori eradication. Successful H. pylori eradication was achieved in 21 patients. The gastric microbiota was characterized using an Illumina MiSeq platform targeting 16S ribosomal DNA (rDNA). The mean follow-up duration was 57.4 months (range, 12–145 months), and median follow-up visit was 1 (range, 1–3). Relative abundance of Lactobacillales and Streptococcus was increased with atrophy/metaplasia. In H. pylori-uninfected subjects (n = 8), an increase in Proteobacteria (Enhydrobacter, Comamonadaceae, Sphingobium); a decrease in Firmicutes (Streptococcus, Veillonella), Fusobacteria (Fusobacterium), Nocardioidaceae, Rothia, and Prevotella; and a decrease in microbial diversity were observed during the follow-up (p trend < 0.05). In 10 of 21 subjects (47.6%), H. pylori eradication induced restoration of microbial diversity; however, a predominance of Acinetobacter with a decrease in microbial diversity occurred in 11 subjects (52.3%). The presence of atrophy/metaplasia at baseline and higher neutrophil infiltration in the corpus were associated with the restoration of gastric microbiota after successful eradication, whereas a higher relative abundance of Acinetobacter at baseline was associated with the predominance of Acinetobacter after H. pylori eradication (p < 0.05). To conclude, in H. pylori-uninfected stomach, relative abundance of Proteobacteria increases, relative abundance of Firmicutes and Fusobacteria decreases, and microbial diversity decreases with aging. H. pylori eradication does not always restore gastric microbiota; in some individuals, gastric colonization by Acinetobacter species occurs after anti-Helicobacter treatment.
Highlights
The stomach is a hostile environment for most bacteria due to high acidity and various antimicrobial chemicals and enzymes
The study participants were classified into four groups: H. pylori-uninfected subjects without evidence of atrophic gastritis and intestinal metaplasia by histology, pepsinogen I/II ratio ≥ 4.0, and no history of H. pylori eradication; H. pylori-infected patients without mucosal atrophy and metaplasia by histology with pepsinogen I/II ratio > 4.0; H. pylori-infected patients with atrophic gastritis and/or intestinal metaplasia by histology and pepsinogen I/II ratio < 2.5; and the subjects with atrophic gastritis and/or intestinal metaplasia, no evidence of current H. pylori infection, anti-H. pylori immunoglobulin G (IgG) antibody negative, and no previous history of H. pylori eradication
We evaluated gastric microbiota profiles according to H. pylori infection and mucosal atrophy/metaplasia in subjects without significant gastrointestinal diseases
Summary
The stomach is a hostile environment for most bacteria due to high acidity and various antimicrobial chemicals and enzymes. H. pylori infection is associated with peptic ulcer diseases, lowgrade gastric mucosa-associated lymphoma, and gastric cancer (GC) (Cover and Blaser, 2009). To prevent these H. pylorirelated diseases, eradication of H. pylori is recommended. Studies on H. pylori eradication have shown that successful eradication alone does not completely prevent the risk of gastric cancer (Correa, 1992; Choi et al, 2018; Li et al, 2019), and it may increase the risk for H. pylori-negative GC (Lee et al, 2019). It has been suggested that factors other than H. pylori contribute to the development of gastric cancer
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