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IL-30, the p28 subunit of IL-27, interacts with the Epstein-Barr virus-induced gene 3 (EBI3) to form IL-27, which modulates the inflammatory responses in autoimmune and infectious diseases. Several previous studies have provided evidence for the role of IL-30 in the anti-inflammatory process. However, the effect of IL-30 in macrophage-mediated immune responses is not well understood. With the recent observation in our experiment, we found that IL-30 exerted potent anti-inflammatory effects in the RAW 264.7 macrophages and in a lipopolysaccharide/D-galactosamine (LPS/D-GalN)-induced mouse model. IL-30 decreased the production of tumor necrosis factor (TNF)-α and IL-6 in LPS-stimulated RAW 264.7 macrophages in a dose-dependent manner. In the macrophage-mediated GalN and LPS model of acute liver injury, IL-30 prevented liver injury by suppressing serum enzyme activity and down-regulating the pro-inflammatory cytokines TNF-α, IL-1β, IL-6, and interferon (IFN)-γ. IL-30 treatment decreased apoptosis in liver tissue and increased glutathione (GSH) levels. We postulated that IL-30 might function through gp130-mediated signaling pathways and then demonstrated that IL-30 affects LPS-induced inflammation through the STAT1, STAT3, and ERK signaling pathways. These data indicate that IL-30 can provide critical protection against macrophage-mediated liver inflammation through anti-apoptotic, anti-oxidant, and anti-inflammatory activities. Copyright © 2013. Published by Elsevier Inc.


Xiao Liu, Zhen Wang, Ning Ye, Zhongwen Chen, Xikun Zhou, Xiu Teng, Nongyu Huang, Ning Liu, Nannan Zhang, Ting Guan, Yongqiu Mao, Bin Kan, Yuquan Wei, Jiong Li. A protective role of IL-30 via STAT and ERK signaling pathways in macrophage-mediated inflammation. Biochemical and biophysical research communications. 2013 May 31;435(2):306-12

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PMID: 23583238

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