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Key Paper Evaluation

Intestinal dysbiosis in irritable bowel syndrome: etiological factor or epiphenomenon?

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Pages 389-393 | Published online: 09 Jan 2014
 

Abstract

Evaluation of: Lyra A, Rinttilä T, Nikkilä J et al. Diarrhoea-predominant irritable bowel syndrome distinguishable by 16S rRNA gene phylotype quantification. World J. Gastroenterol. 15(47), 5936–5945 (2009).

Irritable bowel syndrome (IBS) is a functional disorder of multifactorial origin. Recent interest has been directed to the potential role of intestinal microbiota in the pathophysiology and symptom generation of this syndrome. This hypothesis is supported by the evidence of an infectious trigger in a proportion of patients, the identification of changes in bacterial composition and the detection of antibodies against flagellin, a component of indigenous flora, and by the potential therapeutic modulation of intestinal microbiota with probiotics and nonabsorbable antibiotics in IBS. The study by Lyra et al. assessed fecal microbiota in IBS patients and controls by applying a set of 14 quantitative real-time PCR assays targeting 16S ribosomal RNA gene phylotypes putatively associated with IBS, based on 16S ribosomal RNA gene library sequence analysis. In addition, microbiota composition was investigated over time by applying statistically advanced analyses at three timepoints during 6 months of follow-up. The authors showed that the intestinal flora of patients with diarrhea-predominant IBS diverged significantly not only from controls but also from the other IBS subgroups. The results by Lyra et al. further support the hypothesis that intestinal microbial flora has a role in IBS pathophysiology, and foster the idea that abnormal microbiota may act by triggering local and systemic immune responses linked to symptom generation. Further studies are now needed to clarify the key role of intestinal microbiota (as opposed to a secondary effect) in this common human disease.

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.

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