IL-21 Modulates Release of Proinflammatory Cytokines in LPS-Stimulated Macrophages through Distinct Signaling Pathways. (26th December 2013)

• Record Type: Journal Article
• Authors: Li, Su-nan; Wang, Wei; Fu, Shou-peng; Wang, Jian-fa; Liu, Hong-mei; Xie, Shan-shan; Liu, Bing-run; Li, Yang; Lv, Qing-kang; Li, Zhi-qiang; Xue, Wen-jing; Huang, Bing-xu; Chen, Wei; Liu, Ju-xiong
• Other Names: Denizot Yves Academic Editor.
• Is Part Of: Mediators of inflammation. Volume 2013(2013)
• Publication Date: 2013-12-26
• Subjects: Inflammation -- Mediators -- Periodicals; Biological response modifiers -- Periodicals; Inflammation (Pathologie) -- Médiateurs; Immunomodulateurs; Biological response modifiers; Inflammation -- Mediators; Immunology; Autacoids; Immunologic Factors; Cell Adhesion Molecules; Cell Communication; Cytokines; Inflammation; Periodicals; Electronic journals; 616.0473
• DOI: 10.1155/2013/548073
• Languages: English
• ISSNs: 0962-9351

Abstract

Abstract : 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-1 β, 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 I κ B α phosphorylation and NF- κ B 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- κ B 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.