Correlations of the Gastric and Duodenal Microbiota with Histological, Endoscopic, and Symptomatic Gastritis.

Hye Han,Ji-Hoon Kim,Hyunseok Cho,Sun-Young Lee,Hee Moon,Seo Oh

doi:10.3390/jcm8030312

Abstract

Mucosal inflammation is characterized by neutrophil and mononuclear cell infiltration. This study aimed to determine the gastric and duodenal microbiota associated with histological, endoscopic, and symptomatic gastritis. Dyspeptic adults who presented for evaluation were included. Subjects with either comorbidities or recent drug intake were excluded. Three endoscopic biopsies were obtained from the antrum, body, and duodenum. Next-generation sequencing for 16S ribosomal RNA V1–V2 hypervariable regions was performed. The correlation between the composition of microbiota and the degree of inflammatory cell infiltration, endoscopic findings, and Patient Assessment of Gastrointestinal Disorders Symptom Severity Index (PAGI-SYM) score was analyzed. In 98 included subjects, microbial communities in the antrum and body showed Bray–Curtis similarity; however, those in the duodenum showed dissimilarity. Histological and endoscopic gastritis was associated with the abundance of Helicobacter pylori and that of commensal bacteria in the stomach. The abundances of Variovorax paradoxus and Porphyromonas gingivalis were correlated with histological gastritis, but not with endoscopic or symptomatic gastritis. The total PAGI-SYM score showed a stronger correlation with the duodenal microbiota (Prevotella nanceiensis and Alloprevotella rava) than with the gastric microbiota (H. pylori, Neisseria elongate, and Corynebacterium segmentosum). Different correlations of the gastric and duodenal microbiota with histological, endoscopic, and symptomatic gastritis were observed for the first time at the species level. H. pylori-negative gastritis is not associated with endoscopic or symptomatic gastritis. Only H. pylori-induced endoscopic gastritis requires gastric cancer surveillance. Owing to the weak correlation with H. pylori, symptomatic gastritis should be assessed separately from histological and endoscopic gastritis.

Highlights

Gastritis remains challenging for clinicians, because symptoms may appear even in the absence of histological or endoscopic gastritis
Because the enteric nervous system (ENS) may be regulated by the inflammatory effects of the microbiota resulting in altered symptom sensitivity or cognitive function [33,34], our findings further suggest that the duodenal microbiota (P. nanceiensis and A. rava) and gastric microbiota (H. pylori, N. elongata, and C. segmentosum) may negatively affect ENS modulation via neurogenic inflammatory process
Different correlations of the gastric and duodenal microbiota with histological, endoscopic, and symptomatic gastritis were observed for the first time at the species level

Summary

Introduction

Gastritis remains challenging for clinicians, because symptoms may appear even in the absence of histological or endoscopic gastritis. Owing to the lack of difference between H. pylori-induced organic dyspepsia and functional dyspepsia, histopathological and endoscopic findings are more reliable for diagnosing H. pylori infection and estimating the risk of gastric cancer [2,3]. Aside from H. pylori, other species may induce gastritis; the contribution of other microbiota to symptom generation, mucosal inflammation, and endoscopic findings is still uncertain. Next-generation sequencing (NGS) analysis of the 16S ribosomal RNA (rRNA) hypervariable regions has enabled the understanding of changes in the composition of the gastric microbiota induced by H. pylori infection [5,6]. Recent advances in NGS analysis have enabled the identification of the composition of microbiota in the duodenal mucosa, microbiota other than H. pylori that contribute to mucosal inflammation, carcinogenesis, or symptom generation remain unknown

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