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Curr Treat Options Gastroenterol. 2018 Dec;16(4):591-604. doi: 10.1007/s11938-018-0207-x.

Gastroduodenal "Dysbiosis": a New Clinical Entity.

Author information

1
Department of Gastroenterology and Hepatology, Princess Alexandra Hospital Brisbane, 199 Ipswich Road, Woolloongabba, QLD, 4102, Australia.
2
Faculty of Medicine and Biomedical Sciences, And Faculty of Health and Behavioral Sciences, The University of Queensland, Brisbane, Australia.
3
Translational Research Institute, Brisbane Australia, Microbial Biology and Metagenomics, The University of Queensland Diamantina Institute, Brisbane, Australia.
4
Department of Gastroenterology and Hepatology, Princess Alexandra Hospital Brisbane, 199 Ipswich Road, Woolloongabba, QLD, 4102, Australia. g.holtmann@uq.edu.au.
5
Faculty of Medicine and Biomedical Sciences, And Faculty of Health and Behavioral Sciences, The University of Queensland, Brisbane, Australia. g.holtmann@uq.edu.au.

Abstract

PURPOSE OF REVIEW:

Like the rest of the gastrointestinal tract, the small intestine is colonised by microbes, but how this "microbiome" affects the immune system and digestive functions has largely been overlooked, especially in the "omics" era. Here, we present recent findings that show that the diversity, density and interactions of these microbes in the small intestine can play an important role in the pathogenesis of a number of gastrointestinal and extraintestinal disorders.

RECENT FINDINGS:

Changes in the small intestinal mucosa-associated microbiota (SI-MAM) have been shown to occur with inflammatory bowel diseases, functional gastrointestinal disorders, metabolic disorders such as obesity and type 2 diabetes. More recently, there is emerging evidence that small intestinal dysbiosis can be a driver for the progression of chronic liver disease. Initially believed that small intestinal dysbiosis (e.g. SIBO) is mainly due to alterations of luminal conditions (e.g. after surgical resections of the ileocecal valve), there is now enough evidence to conclude that small intestinal dysbiosis can occur without underlying structural abnormalities. Alterations of the SI-MAM appear to play a key role for the manifestation and progression of inflammatory and metabolic disorders.

KEYWORDS:

Microbiome; Microbiota; Small intestine

PMID:
30421297
DOI:
10.1007/s11938-018-0207-x

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