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The urge of deciphering the secrets of gut microbiota has pervaded merely all fields of medicine, including that of functional GI disorders, now called disorders of gut brain interaction (DGBI).1 The concept that gut microbiota could contribute to symptom generation in DGBI, particularly in IBS is not new. Dysbiosis, small intestinal bacterial overgrowth and bacterial fermentation of foods have been suspected for a long time, although never demonstrated with certainty due to methodological limitations.1 Nonetheless, convincing indirect evidence links microorganisms and microbiota to IBS. Indeed, a bout of infection gastroenteritis leads to the development of IBS in 1 in 10 subjects, the so-called postinfection IBS,2 and disruption of the gut ecosystem with systemic antibiotics increases the risk of IBS.3 With the advent of next-generation sequencing technology and bioinformatics, altered microbiota profiles could be finally detected in patients with IBS compared with healthy individuals.1 However, the disappointment that a unifying microbiological hypothesis did not hold true in all patients was just around the corner.4 In addition, the dilemma if the described microbiota changes are consequence rather than cause of gut dysfunction has never been resolved.1 While rigorous mechanistic studies have yet provided a clear rationale for therapeutic intervention, scientists have been tempted to take shortcuts and point directly to microbiota modulation. In IBS, this approach has been somewhat rewarding. Dietary manipulation reducing fermentable substrates for the microbiota (ie, low-FODMAP diets), downregulation of pathobionts and upregulation of beneficial bacteria (eg, lactobacilli and bifidobacteria) with non-absorbable antibiotics or the use of probiotics have shown some degree of improvement of IBS symptoms.5
Faecal microbiota transplantation (FMT) is undoubtedly the most powerful modality available in the hands of physicians to replace …
Contributors GB and GI equally contributed to the writing of the paper.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent for publication Not required.
Provenance and peer review Commissioned; internally peer reviewed.
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