[HTML][HTML] IL-17A induces pro-inflammatory cytokines production in macrophages via MAPKinases, NF-κB and AP-1

J Chen, M Liao, X Gao, Q Zhong, T Tang, X Yu… - Cellular Physiology and …, 2013 - karger.com
J Chen, M Liao, X Gao, Q Zhong, T Tang, X Yu, Y Liao, X Cheng
Cellular Physiology and Biochemistry, 2013karger.com
Background: Interleukin (IL)-17A, a newly identified cytokine, may participate in the transition
of a stable plaque into an unstable plaque. Macrophages play a critical role in the
destabilization of atherosclerotic plaque. Methods: RAW 264.7 cells were stimulated with IL-
17A. The mRNA expression of inflammatory cytokines was determined by RT-PCR. The
cytokines production in the supernatants was measured by ELISA. Small interfering RNA
(siRNA) was used to confirm that IL-17A-induced pro-inflammatory cytokines production via …
Background
Interleukin (IL)-17A, a newly identified cytokine, may participate in the transition of a stable plaque into an unstable plaque. Macrophages play a critical role in the destabilization of atherosclerotic plaque.
Methods
RAW 264.7 cells were stimulated with IL-17A. The mRNA expression of inflammatory cytokines was determined by RT-PCR. The cytokines production in the supernatants was measured by ELISA. Small interfering RNA (siRNA) was used to confirm that IL-17A-induced pro-inflammatory cytokines production via IL-17RA signaling. The western blot assay was used to detect the phosphorylation of MAPKinases including p38 and ERK1/2. The DNA binding activity of nuclear factor NF-κB and AP-1 were detected by EMSA.
Results
IL-17A induced the production of pro-inflammatory cytokines in macrophages in a time-and dose-dependent manner, such as tumor necrosis factor (TNF)-a, IL-1ß, and IL-6. Meanwhile, IL-17A resulted in the phosphorylation of p38 and ERK1/2 and increased DNA-binding activity of NF-κB and AP-1. Pharmacological inhibitors of p38 and ERK1/2 partly attenuated IL-17A-induced TNF-a, IL-1ß, and IL-6 production. Either NF-κB inhibitor or AP-1 inhibitor also partly decreased the IL-17A-induced cytokine production.
Conclusions
IL-17A induces pro-inflammatory cytokines production in macrophages via MAPKinases, NF-κB and AP-1 pathway.
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