IL-21 modulates release of proinflammatory cytokines in LPS-stimulated macrophages through distinct signaling pathways.

IL-21 modulates release of proinflammatory cytokines in LPS-stimulated macrophages through distinct signaling pathways.
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IL-21 通过不同的信号通路调节 LPS 刺激的巨噬细胞中促炎细胞因子的释放

DOI:
10.1155/2013/548073
复制
发表时间:
2013
影响因子:
4.6
通讯作者:
Liu JX
Liu JX
中科院分区:
医学3区
文献类型:
--
作者:
Li SN;Wang W;Fu SP;Wang JF;Liu HM;Xie SS;Liu BR;Li Y;Lv QK;Li ZQ;Xue WJ;Huang BX;Chen W;Liu JX

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本研究旨在探讨IL-21对lps诱导的小鼠腹腔巨噬细胞的抗炎作用。结果表明,IL-21显著抑制lps诱导的巨噬细胞IL-1β、TNF-α和IL-6 mRNA的表达,但对IFN-γ、IL-10、CCL5和CXCL2的mRNA表达无明显抑制作用。ELISA分析显示,IL-21还能抑制lps诱导的培养上清中TNF-α和IL-6的产生。Western blot分析显示,IL-21明显抑制lps刺激的巨噬细胞ERK和i -κB α磷酸化和NF-κB易位,但增加STAT3磷酸化。流式细胞术和Western blot分析显示,IL-21降低了lps刺激细胞中M1巨噬细胞表面标志物CD86、iNOS和TLR4的表达。所有结果表明,IL-21通过抑制ERK的磷酸化和NF-κB的易位来减少IL-6和TNF-α的产生,并通过降低CD86、iNOS和TLR4的表达以及增加lps刺激细胞中STAT3的磷酸化来促进巨噬细胞从M1向M2表型的转变。
The aim of this study was to investigate the anti-inflammatory effect of IL-21 on LPS-induced mouse peritoneal macrophages. The results showed that IL-21 significantly inhibited LPS-induced mRNA expression of IL-1β, TNF-α, and IL-6 in macrophages, but not of IFN-γ, IL-10, CCL5, or CXCL2. ELISA analysis showed that IL-21 also suppressed LPS-induced production of TNF-α and IL-6 in culture supernatants. Western blot analysis showed that IL-21 clearly inhibited ERK and IκBα phosphorylation and NF-κB translocation in LPS-stimulated macrophages, but it increased STAT3 phosphorylation. Flow cytometric and Western blot analysis showed that IL-21 decreased M1 macrophages surface markers expression of CD86, iNOS, and TLR4 in LPS-stimulated cells. All results suggested that IL-21 decreases IL-6 and TNF-α production via inhibiting the phosphorylation of ERK and translocation of NF-κB and promotes a shift from the M1 to M2 macrophage phenotype by decreasing the expression of CD86, iNOS, and TLR4 and by increasing STAT3 phosphorylation in LPS-stimulated cells.
姜黄素消除了LPS诱导的264.7巨噬细胞中的促炎细胞因子。涉及SOCS -1,-3和P38 MAPK的新型机制的证据。
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