It is increasingly perceived that gut host–microbial interactions are important elements in the pathogenesis of functional gastrointestinal disorders (FGID). The most convincing evidence to date is the finding that functional dyspepsia and irritable bowel syndrome (IBS) may develop in predisposed individuals following a bout of infectious gastroenteritis. There has been a great deal of interest in the potential clinical and therapeutic implications of small intestinal bacterial overgrowth in IBS. However, this theory has generated much debate because the evidence is largely based on breath tests which have not been validated. The introduction of culture-independent molecular techniques provides a major advancement in our understanding of the microbial community in FGID. Results from 16S rRNA-based microbiota profiling approaches demonstrate both quantitative and qualitative changes of mucosal and faecal gut microbiota, particularly in IBS. Investigators are also starting to measure host–microbial interactions in IBS. The current working hypothesis is that abnormal microbiota activate mucosal innate immune responses which increase epithelial permeability, activate nociceptive sensory pathways and dysregulate the enteric nervous system. While we await important insights in this field, the microbiota is already a therapeutic target. Existing controlled trials of dietary manipulation, prebiotics, probiotics, synbiotics and non-absorbable antibiotics are promising, although most are limited by suboptimal design and small sample size. In this article, the authors provide a critical review of current hypotheses regarding the pathogenetic involvement of microbiota in FGID and evaluate the results of microbiota-directed interventions. The authors also provide clinical guidance on modulation of gut microbiota in IBS.
- Functional gastrointestinal disorders
- irritable bowel syndrome
- small intestinal bacterial overgrowth
- breath tests
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Funding This work is supported by Rome Foundation, USA. In addition, the authors would like to acknowledge the following funding sources: Italian Ministry of Education, University and Research (PRIN 2009); Fondazione Cassa di Risparmio and IMA, Bologna, Italy (GB); Scottish government RESAS support (HJF); The Swedish Medical Research Council (grants 13409, 21691 and 21692), the Marianne and Marcus Wallenberg Foundation, and the University of Gothenburg, Centre for Person-Centred Care (GPCC), Sahlgrenska Academy, University of Gothenburg and by the Faculty of Medicine, University of Gothenburg (MS); Shire/Movetis, Amgen, Ironwood (BS); Canadian Institute of Health Research (CIHR) and Crohn's and Colitis Foundation of Canada (CCFC) (SV); Lesaffre International, Norgine, National Institute for Health Research Biomedical Research Unit Grant (RS); CAG/CIHR, CCA (Canadian Celiac Association), CCFC and Nestec (EFV); EFV holds a Career Award from the Department of Medicine, McMaster University.
Competing interests This is a Rome Working Team Report. All authors are responsible for writing the study interpretation of data, and critical revision of the manuscript. The authors would like to disclose the following potential competing interests: Alfa-Wasserman, Prometheus, Shire/Movetis, Sofar (GB); Danone Research, Arla Foods, Novartis, Shire/Movetis, AstraZeneca (MS); Ironwood, Shire/Movetis, Prometheus (BS); Boeringer Ingelheim & Ironwood (RS); Ferring Canada and US (SV); Nestec grant support (EFV); Novartis Pharmaceuticals, GlaxoSmithKline, Solvay Pharmaceuticals, Pfizer Global Research and Development, Rotta Research, Proctor and Gamble, Danone Research, Astellas Pharma, Ironwood Pharmaceuticals, Sucampo Pharmaceuticals, Almirall Pharma, Movetis UK, Norgine, Chr Hansen, Boehringer-Ingelheim, and Heel GMBH (PW).
Provenance and peer review Not commissioned; externally peer reviewed.
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