Oral and gastric microbiome in relation to gastric intestinal metaplasia

Evidence suggests that Helicobacter pylori plays a role in gastric cancer (GC) initiation. However, epidemiologic studies on the specific role of other bacteria in the development of GC are lacking. We conducted a case‐control study of 89 cases with gastric intestinal metaplasia (IM) and 89 matched controls who underwent upper gastrointestinal endoscopy at three sites affiliated with NYU Langone Health. We performed shotgun metagenomic sequencing using oral wash samples from 89 case‐control pairs and antral mucosal brushing samples from 55 case‐control pairs. We examined the associations of relative abundances of bacterial taxa and functional pathways with IM using conditional logistic regression with and without elastic‐net penalty. Compared with controls, oral species Peptostreptococcus stomatis, Johnsonella ignava, Neisseria elongata and Neisseria flavescens were enriched in cases (odds ratios [ORs] = 1.29‐1.50, P = .004‐.01) while Lactobacillus gasseri, Streptococcus mutans, S parasanguinis and S sanguinis were under‐represented (ORs = 0.66‐0.76, P = .006‐.042) in cases. Species J ignava and Filifactor alocis in the gastric microbiota were enriched (ORs = 3.27 and 1.43, P = .005 and .035, respectively), while S mutans, S parasanguinis and S sanguinis were under‐represented (ORs = 0.61‐0.75, P = .024‐.046), in cases compared with controls. The lipopolysaccharide and ubiquinol biosynthesis pathways were more abundant in IM, while the sugar degradation pathways were under‐represented in IM. The findings suggest potential roles of certain oral and gastric microbiota, which are correlated with regulation of pathways associated with inflammation, in the development of gastric precancerous lesions. What's new? There's not much evidence for how gut bacteria, besides H. pylori, contribute to gastric cancer risk. Here, the authors used metagenome sequencing to characterize the differences in bacterial microbiota in gastric precancerous lesion cases compared with healthy controls. In gastric intestinal metaplasias, they found higher proportions of several species related to periodontal disease as well as opportunistic pathogens, but lower levels of certain commensals and probiotic species. Metagenomic analysis revealed pathways that were associated with gastric intestinal metaplasias, suggesting a possible mechanism for how the bacteria influence disease risk.