Interleukin-6 plays a crucial role in the hepatic expression of SOCS3 during acute inflammatory processes in vivo

摘要: Background/Aims Interleukin-6 is mandatory for liver regeneration after injury and the hepatic expression of acute phase proteins cytochrome P450 enzymes during inflammation. Due to its crucial contribution maintenance homeostasis IL-6 signaling tightly controlled. Suppressor cytokine (SOCS) 3 a potent IL-6-induced feedback inhibitor terminating signal transduction. However, several pathways converge on SOCS3: SOCS3 can be induced by other mediators in vitro, it does not exclusively inhibit signaling. The individual each induction vivo unknown. Methods Using IL-6-deficient mice we analyzed role interleukin-6 response turpentine LPS as models aseptic bacterial inflammation, respectively. Results In wild-type animals, elicited strong SOCS3. mice, contrast, showed severely impaired both stimuli: failed induce mRNA; LPS-induced early inductive 60min injection was absent, delayed markedly reduced. residual abolished IL-6/TNFR-1 knockout mice. Conclusions Our data strongly argue inflammatory processes vivo. Although cytokines are capable inducing their seems minor.