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Gut. 2018 Jun;67(6):1024-1032. doi: 10.1136/gutjnl-2017-314281. Epub 2017 Aug 1.

Mucosal microbiome dysbiosis in gastric carcinogenesis.

Author information

1
Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong, China.
2
State Key Laboratory of Cancer Biology, Xijing Hospital, Fourth Military Medical University, Xian, China.
3
Department of Gastroenterology and Hepatology, Inner Mongolia People's Hospital, Hohhot, China.
4
Department of Microbiology, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China.

Abstract

OBJECTIVES:

We aimed to characterise the microbial changes associated with histological stages of gastric tumourigenesis.

DESIGN:

We performed 16S rRNA gene analysis of gastric mucosal samples from 81 cases including superficial gastritis (SG), atrophic gastritis (AG), intestinal metaplasia (IM) and gastric cancer (GC) from Xi'an, China, to determine mucosal microbiome dysbiosis across stages of GC. We validated the results in mucosal samples of 126 cases from Inner Mongolia, China.

RESULTS:

We observed significant mucosa microbial dysbiosis in IM and GC subjects, with significant enrichment of 21 and depletion of 10 bacterial taxa in GC compared with SG (q<0.05). Microbial network analysis showed increasing correlation strengths among them with disease progression (p<0.001). Five GC-enriched bacterial taxa whose species identifications correspond to Peptostreptococcus stomatis, Streptococcus anginosus, Parvimonas micra, Slackia exigua and Dialister pneumosintes had significant centralities in the GC ecological network (p<0.05) and classified GC from SG with an area under the receiver-operating curve (AUC) of 0.82. Moreover, stronger interactions among gastric microbes were observed in Helicobacter pylori-negative samples compared with H. pylori-positive samples in SG and IM. The fold changes of selected bacteria, and strengths of their interactions were successfully validated in the Inner Mongolian cohort, in which the five bacterial markers distinguished GC from SG with an AUC of 0.81.

CONCLUSIONS:

In addition to microbial compositional changes, we identified differences in bacterial interactions across stages of gastric carcinogenesis. The significant enrichments and network centralities suggest potentially important roles of P. stomatis, D. pneumosintes, S. exigua, P. micra and S. anginosus in GC progression.

KEYWORDS:

Gastric cancer; mucosal microbiome dysbiosis; oral bacteria

PMID:
28765474
PMCID:
PMC5969346
DOI:
10.1136/gutjnl-2017-314281
[Indexed for MEDLINE]
Free PMC Article

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