Contentious host–microbiota relationship in inflammatory bowel disease – can foes become friends again?

Abstract

Inflammatory bowel diseases (IBDs) are chronic debilitating disorders of unknown etiology, consisting of two main conditions, ulcerative colitis and Crohn’s disease. Major advances have recently taken place in human genetic studies of IBD and over 160 risk loci for these two diseases have been uncovered. These genetic data highlight a key role for genes that code for immunological and epithelial barrier functions. Environmental factors also make substantial contributions to the pathogenesis of IBD and account for the growing incidence of the diseases around the world. Intestinal microbiota creates resistance to infection, provides nutrients, and educates the immune system and in many ways has a significant impact on human health. Aberrant microbiota composition and decreased diversity (dysbiotic microbiota) are key etiopathological events in IBD. Dysbiotic microbiota can lead to loss of normal, regulatory immune effects in the gut mucosa. This may play a central role in the development and perpetuation of chronic inflammation. Further, the expression of specific innate immune receptors that recognize microbes is altered in the IBD epithelium. Therefore, the combination of host side epithelial barrier functions and the presence of dysbiotic microbiota in the gut together promote inflammation. New therapeutic options targeting microbiota are currently considered for IBD and they may, in the future, provide means to reverse the pathogenic host–microbiota relationship into a symbiotic one. In this review, the focus is on the intestinal microbiota and host–microbe interactions in IBD.

Key Words:

• anti-inflammatory bacteria
• chronic inflammation
• Crohn’s disease
• host–microbe interaction
• microbiota
• microbiota dysbiosis
• proinflammatory bacteria
• ulcerative colitis

Acknowledgments

The author thanks the Academy of Finland (grants 138902 and 258439) and the Finnish Foundation for Gastroenterological Research for the financial support. The work was independent of the funding.

Declaration of interest: The author reports no conflicts of interest. The author alone is responsible for the content and writing of the paper.