Copyright ©The Author(s) 2021.
World J Gastroenterol. Jun 14, 2021; 27(22): 3010-3021
Published online Jun 14, 2021. doi: 10.3748/wjg.v27.i22.3010
Table 1 Bile acids regulate host immunological homeostasis and inflammatory response
Microbial bile acid metabolites modulate gut RORγ+ regulatory T cell homeostasisSong et al[83], 2020BA nuclear receptorsRestoration of the intestinal BA pool can increase colonic RORγ+ Treg cell counts and ameliorate host susceptibility to inflammatory colitis
Bile acid metabolites control Th17 and Treg cell differentiationHang et al[48], 2019Derivatives of LCA, 3-oxoLCA and isoalloLCAAdministration of 3-oxoLCA and isoalloLCA to mice reduced Th17 cell differentiation and increased Treg cell differentiation, respectively, in the intestinal lamina propria
Bile acids control inflammation and metabolic disorder through inhibition of NLRP3 inflammasomeGuo et al[26], 2016Membrane receptor TGR5Bile acids inhibited activation of the NLRP3 inflammasome via the TGR5-cAMP-PKA axis.
Gut microbiome–mediated bile acid metabolism regulates liver cancer via NKT cellsMa et al[10], 2018Hepatic CXCR6+ NKT cellsMicrobiome uses bile acids as a messenger to accumulate NKT cells, which have an activated phenotype and inhibit liver tumor growth.
TGR5 activation inhibits atherosclerosis by reducing macrophage inflammation and lipid loadingPols et al[77], 2011Membrane receptor TGR5TGR5 activation in macrophages by 6a-ethyl-23(S)-methylcholic acid (6-EMCA, INT-777), a semisynthetic BA, inhibits proinflammatory cytokine production, an effect mediated by TGR5-induced cAMP signaling and subsequent NF-κB inhibition.