Effect of gut flora mediated‐bile acid metabolism on intestinal immune microenvironment

Abstract

According to reports, gut microbiota and metabolites regulate the intestinal immune microenvironment. In recent years, an increasing number of studies reported that bile acids (BAs) of intestinal flora origin affect T helper cells and regulatory T cells (Treg cells). Th17 cells play a pro‐inflammatory role and Treg cells usually act in an immunosuppressive role. In this review, we emphatically summarised the influence and corresponding mechanism of different configurations of lithocholic acid (LCA) and deoxycholic acid (DCA) on intestinal Th17 cells, Treg cells and intestinal immune microenvironment. The regulation of BAs receptors G protein‐coupled bile acid receptor 1 (GPBAR1/TGR5) and farnesoid X receptor (FXR) on immune cells and intestinal environment are elaborated. Furthermore, the potential clinical applications above were also concluded in three aspects. The above will help researchers better understand the effects of gut flora on the intestinal immune microenvironment via BAs and contribute to the development of new targeted drugs.

FXR Friend-ChIPs in the Enterohepatic System

“… 26 Bacteria create secondary bile acids via deconjugation, dihydroxylation at carbon 7, oxidation, and epimerization of primary bile acids to dampen antimicrobial function, alter intestinal immune microenvironment, and improve bacterial fitness. 26 27 …”

“…26 Bacteria create secondary bile acids via deconjugation, dihydroxylation at carbon 7, oxidation, and epimerization of primary bile acids to dampen antimicrobial function, alter intestinal immune microenvironment, and improve bacterial fitness. 26,27 In the liver, circulating FGF15/FGF19 binds to hepatic β-klotho and FGF receptor 4 dimer to inhibit gene expression of cytochrome P450 7a1 (Cyp7a1/CYP7A1) and 8b1 (Cyp8b1/ CYP8B1), ultimately suppressing bile acid synthesis. 13,14,28,29 Circulating bile acids activate hepatic FXR leading to induction of SHP that mainly functions to inhibit Cyp8b1 expression.…”