The microbiome in inflammatory bowel diseases: from pathogenesis to therapy

Abstract

Inflammatory bowel disease (IBD) has become a global disease with accelerating incidence worldwide in the 21st century while its accurate etiology remains unclear. In the past decade, gut microbiota dysbiosis has consistently been associated with IBD. Although many IBD-associated dysbiosis have not been proven to be a cause or an effect of IBD, it is often hypothesized that at least some of alteration in microbiome is protective or causative. In this article, we selectively reviewed the hypothesis supported by both association studies in human and pathogenesis studies in biological models. Specifically, we reviewed the potential protective bacterial pathways and species against IBD, as well as the potential causative bacterial pathways and species of IBD. We also reviewed the potential roles of some members of mycobiome and virome in IBD. Lastly, we covered the current status of therapeutic approaches targeting microbiome, which is a promising strategy to alleviate and cure this inflammatory disease.

Keywords: dysbiosis; etiology; inflammatory bowel disease; microbiome; pathogenesis; therapy.

Figure 1

Graphical summary of potentially protective and causative microbial bacterial pathways and species in IBD. SCFAs, tryptophan derivatives, secondary BAs and PSA gene expression are found depleted in human IBD gut. They are also proved to have anti-inflammatory effects in biological models and therefore are often proposed as protective factors. Prebiotics, probiotics or postbiotics targeting these factors are promising strategies to alleviate IBD. In contrast, taurine is found enriched in the metabolome and virulent genes are found enriched in microbiome of human IBD gut. Taurine and the virulence-gene-containing pathobionts also have pro-inflammatory effects in biological models and therefore are proposed as potentially causative factor for IBD. Phage therapies that target these factors are promising strategies to alleviate IBD. SCFAs, short-chain fatty acids; SBAs, secondary bile acids; PSA, polysaccharide A