Objective Patients infected with Helicobacter pylori develop chronic gastritis with a subgroup progressing to further complications. The role of microbiota from the oral cavity swallowed with saliva and either transiting the stomach or persisting in the gastric mucosa is uncertain. It is also not known whether the bacterial community differs in luminal and mucosal niches. A key question is whether H. pylori influences the bacterial communities of gastroduodenal niches.
Design Saliva, gastric and duodenal aspirates as well as gastric and duodenal biopsies were collected during oesophagogastroduodenoscopy from 24 patients (m:9, f:15, mean age 52.2±SD 14.5 years). RNA was extracted and the V1–V2 region of the retrotranscribed bacterial 16S rRNA amplified and sequenced on the Illumina MiSeq platform.
Results Overall, 687 bacterial phylotypes that belonged to 95 genera and 11 phyla were observed. Each individual comprised a unique microbiota composition that was consistent across the different niches. However, the stomach fluid enriched for specific microbiota components. Helicobacter spp were shown to dominate the mucosa-associated community in the stomach, and to significantly influence duodenal and oral communities.
Conclusions The detailed analysis of the active global bacterial communities from the five distinct sites of the upper GI tract allowed for the first time the differentiation between host effects and the influence of sampling region on the bacterial community. The influence of Helicobacter spp on the global community structures is striking.
- BACTERIAL INTERACTIONS
- HELICOBACTER PYLORI
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Contributors DHP, PM and CS contributed to the study design, analysis and interpretation of the data. DHP and CS drafted the manuscript. CS, KS and PM collected samples and identified suitable subjects. DHP and PM supervised the study procedures. CS, NK and APAO established analyses and performed laboratory workup. MV, DHP, MLW-O and RV-V performed bioinformatic and statistical analyses. All authors read and approved the final version of the manuscript.
Funding This study was supported by iMed, the Helmholtz Association's Initiative on Personalized Medicine. CS was supported by CRC854, a research programme by the German funding organisation DFG.
Competing interests None.
Ethics approval University of Magdeburg operation number 31/11.
Provenance and peer review Not commissioned; externally peer reviewed.