Gut microbiota and irritable bowel syndrome

Irritable bowel syndrome (IBS) is a common gastrointestinal disorder that poses a significant health concern. Although its etiology remains unknown, there is growing evidence that gut dysbiosis is involved in the development and exacerbation of IBS. Previous studies have reported altered microbial diversity, abundance, and composition in IBS patients when compared to controls. However, whether dysbiosis or aberrant changes in the intestinal microbiota can be used as a hallmark of IBS remains inconclusive. We reviewed the literatures on changes in and roles of intestinal microbiota in relation to IBS and discussed various gut microbiota manipulation strategies. Gut microbiota may affect IBS development by regulating the mucosal immune system, brain-gut-microbiome interaction, and intestinal barrier function. The advent of high-throughput multi-omics provides important insights into the pathogenesis of IBS and promotes the development of individualized treatment for IBS. Despite advances in currently available microbiota-directed therapies, large-scale, well-organized, and long-term randomized controlled trials are highly warranted to assess their clinical effects. Overall, gut microbiota alterations play a critical role in the pathophysiology of IBS, and modulation of microbiota has a significant therapeutic potential that requires to be further verified.

Automated summary

Gut dysbiosis is likely involved in the development of irritable bowel syndrome (IBS) and may affect it through regulating the mucosal immune system, brain-gut-microbiome interaction, and intestinal barrier function. While it remains inconclusive whether dysbiosis can be used as a hallmark of IBS, the advent of high-throughput multi-omics provides important insights into IBS pathogenesis and promotes individualized treatment development. Despite advances in microbiota-directed therapies, large-scale, well-organized, and long-term randomized controlled trials are needed to assess their clinical effects.