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 -