Differential modulation of interleukin 8 by interleukin 4 and interleukin 10 in HepG2 cells treated with acetaldehyde
Article first published online: 7 FEB 2005
Volume 25, Issue 1, pages 122–130, February 2005
How to Cite
Gómez-Quiroz, L. E., Paris, R., María Lluis, J., Bucio, L., Souza, V., Hernández, E., Gutiérrez, M., Santiago, M., García-Ruiz, C., Fernández-Checa, J. C., Kershenobich, D. and Gutiérrez-Ruiz, Ma. C. (2005), Differential modulation of interleukin 8 by interleukin 4 and interleukin 10 in HepG2 cells treated with acetaldehyde. Liver International, 25: 122–130. doi: 10.1111/j.1478-3231.2005.01005.x
- Issue published online: 7 FEB 2005
- Article first published online: 7 FEB 2005
- Received 24 March 2004, accepted 11 July 2004
Abstract: Background/Aim: Pro-inflammatory cytokines and chemokines, such as interleukin (IL) 8, are important mediators of hepatic injury and repair following an insult. The purpose of this work was to study the regulation of IL-8 by IL-10 and IL-4 in HepG2 cells treated with acetaldehyde (Ac). Methods: HepG2 cells were pretreated with IL-10 or IL-4 before exposure to Ac, examining IL-8 expression by reverse transcription polymerase chain reaction and Western blot.
Results: Ac treatment produced an increment in IL-8 induction and secretion that was prevented by IL-4 pretreatment, while IL-10 pretreatment failed to decrease Ac-induced IL-8 production. Consistent with these findings Ac increased NF-κB and AP-1 activation that were prevented by IL-4 but not by IL-10, findings accompanied by greater IκB-α levels in IL-4 but not IL-10 pretreated cells. In contrast to the pro-inflammatory role of IL-10 in HepG2, IL-10 did not show any change in the activation of NF-κB by Ac in WRL-68 cells, a human fetal hepatic cell line. Moreover, IL-10 did not induce the degradation of IκB-α in cellular extract from rat primary cultured cells.
Conclusions: While the present findings demonstrate the anti-inflammatory role of IL-4 in preventing the expression of IL-8 by Ac, the regulation of chemokines by anti-inflammatory cytokines is complex and depends on the cellular lineage.