Bilirubin blocks TLR4 signaling by scavenging NADPH oxidase-derived reactive oxygen species.
Bilirubin specifically inhibits the TRIF-dependent TLR4 signaling pathway.
LPS activation of inducible nitric oxide synthase is mediated by HIF-1α.
Macrophages exhibit reciprocal regulation of HIF-1α and aryl hydrocarbon receptor pathways.
Potential mechanisms underlying the anti-inflammatory effects of bilirubin are delineated.