| First Author | Feng D | Year | 2009 |
| Journal | Biochem Pharmacol | Volume | 77 |
| Issue | 2 | Pages | 277-84 |
| PubMed ID | 18940183 | Mgi Jnum | J:144654 |
| Mgi Id | MGI:3831473 | Doi | 10.1016/j.bcp.2008.09.028 |
| Citation | Feng D, et al. (2009) Interleukin 10 deficiency exacerbates halothane induced liver injury by increasing interleukin 8 expression and neutrophil infiltration. Biochem Pharmacol 77(2):277-84 |
| abstractText | The prediction and prevention of drug-induced liver injury (DILI) have been hindered by limited knowledge of the underlying mechanisms, in part the result of a lack of animal models. Using a newly established DILI model induced by halothane, we found increased liver damage susceptibility in interleukin 10 (IL-10) knockout (KO) mice. Extensive neutrophil infiltration and chemoattractant factor interleukin 8 (IL-8) expression in IL-10 KO mice were observed after halothane administration. The elevation of IL-8 expression was NF-kappaB- and P38 MAPK-dependent. In addition, increased signal transducer and activator of transcription factors (STAT) 1 and STAT3 were observed in halothane treated IL-10 KO mice. Exogenous IL-10 treatment protected susceptible mice from halothane induced liver injury (HILI). In conclusion, IL-10 deficiency increases susceptibility to HILI and increased IL-8 expression as well as neutrophil infiltration may be responsible for this phenomenon. |
