TY - JOUR A2 - Denizot, Yves AU - Li, Su-nan AU - Wang, Wei AU - Fu, Shou-peng AU - Wang, Jian-fa AU - Liu, Hong-mei AU - Xie, Shan-shan AU - Liu, Bing-run AU - Li, Yang AU - Lv, Qing-kang AU - Li, Zhi-qiang AU - Xue, Wen-jing AU - Huang, Bing-xu AU - Chen, Wei AU - Liu, Ju-xiong PY - 2013 DA - 2013/12/26 TI - IL-21 Modulates Release of Proinflammatory Cytokines in LPS-Stimulated Macrophages through Distinct Signaling Pathways SP - 548073 VL - 2013 AB - 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. SN - 0962-9351 UR - https://doi.org/10.1155/2013/548073 DO - 10.1155/2013/548073 JF - Mediators of Inflammation PB - Hindawi Publishing Corporation KW - ER -