IL-21 Modulates Release of Proinflammatory Cytokines in LPS-Stimulated Macrophages through Distinct Signaling Pathways

• Main Authors: Su-nan Li (Author), Wei Wang (Author), Shou-peng Fu (Author), Jian-fa Wang (Author), Hong-mei Liu (Author), Shan-shan Xie (Author), Bing-run Liu (Author), Yang Li (Author), Qing-kang Lv (Author), Zhi-qiang Li (Author), Wen-jing Xue (Author), Bing-xu Huang (Author), Wei Chen (Author), Ju-xiong Liu (Author)
• Format: Book
• Published: Hindawi Limited, 2013-01-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.

Summary

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.

Item Description

0962-9351
1466-1861
10.1155/2013/548073