Table 1.

The effects of bile acids on inflammatory mediators in cholestatic liver injury depends upon cell type

Cell type	Bile acid species	Response	Mediator/pathway	References
Mouse hepatocytes	TCA, DCA. CDCA, Bile	Induction of inflammatory cytokines	MAPKs/Egr1	10, 11
Mouse and human hepatocytes	Major endogenous bile acids	Induction of inflammatory cytokines, neutrophil chemotaxis	ER stress, Mitochondrial damage, Tlr9 activation.	18
Mouse cholangiocytes	BDL model	Secretion and cleavage of osteopontin for immune cell recruitment Cell proliferation	Excessive pressure in the biliary system/MMPs TGR5/cSrc-EGFR-MEK-ERK1/2	48, 54, 61
	TLCA, TCA	Activation of COX-2	S1PR2/ERK1/2/NF-kB
Mouse and human neutrophils	BDL model	Activation, chemotaxis and cytotoxicity	DAMPs CXC/CCL chemokines Adhesion molecules Cytoskeletal proteins	16–18, 72–74, 80, 82
Mouse and human monocytes/macrophages	BDL model TC, TCDC, GCDC, TLCA, CDCA	Production of pro-or/and anti-inflammatory cytokines	TGR5/NF-kB/JNK/Inflammasome	50, 56, 87–92, 103
Mouse TH cells	BDL model	Production of pro- inflammatory and fibrotic cytokine IL-17		93, 97
Mouse NK and invariant NK T cells	BDL model	Stimulation of anti- or suppression of pro- inflammatory cytokines produced in Kupffer cells		98, 99