The interplay between host immune cells and gut microbiota in chronic inflammatory diseases

Abstract

Many benefits provided by the gut microbiota to the host rely on its intricate interactions with host cells. Perturbations of the gut microbiota, termed gut dysbiosis, affect the interplay between the gut microbiota and host cells, resulting in dysregulation of inflammation that contributes to the pathogenesis of chronic inflammatory diseases, including inflammatory bowel disease, multiple sclerosis, allergic asthma and rheumatoid arthritis. In this review, we provide an overview of how gut bacteria modulates host metabolic and immune functions, summarize studies that examined the roles of gut dysbiosis in chronic inflammatory diseases, and finally discuss measures to correct gut dysbiosis as potential therapeutics for chronic inflammatory diseases.

Figure 1

Functions of the microbiota in host metabolism. Some bacterial enzymes are capable of converting food- and host-derived carbohydrates to simple carbohydrates in the colon. Gut symbiotic bacteria such as Bifidobacteria and Lactobacilli are able to synthesize vitamin K and water-soluble vitamin B. SCFAs also are produced from diet fibers by Bacteroides, and used as nutrients, energy source and signaling molecules. SCFA, short-chain fatty acid.

Figure 2

Symbionts directly and indirectly regulate the growth and colonization of pathobionts and pathogens. Symbionts outcompete pathobionts and pathogens by consuming limited nutrients, producing bacteriocins and lowering luminal pH through SCFA production. SCFAs and byproducts produced by symbionts regulate the expression of virulence genes in the pathobionts and pathogens. Moreover, symbionts elicit the host immune responses, such as recruitment of neutrophils, cytokine production of macrophages, differentiation of T_H17, ILC3 and Treg cells, IgA production by B cells, and antimicrobial peptides production from epithelial cells. SCFA, short-chain fatty acid.