Inhibition of joint inflammation and destruction induced by anti-type II collagen antibody/lipopolysaccharide (LPS)-induced arthritis in mice due to deletion of macrophage migration inhibitory factor (MIF)
Inhibition of joint inflammation and destruction induced by anti-type II collagen antibody/lipopolysaccharide (LPS)-induced arthritis in mice due to deletion of macrophage migration inhibitory factor (MIF)
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DOI：
10.1016/j.cyto.2004.02.007
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发表时间：
2004-06-07
期刊：
影响因子：
3.8
通讯作者：
Tohyama, H
中科院分区：
文献类型：
--
作者：
Ichiyama, H;Onodera, S;Tohyama, H
目的：先前的研究表明，抗巨噬细胞迁移抑制因子（MIF）抗体中和巨噬细胞迁移抑制因子（MIF）可减少胶原诱导关节炎模型中关节的破坏。本研究旨在探讨选择性删除MIF是否能抑制小鼠抗II型胶原抗体(anti-CII Ab)/脂多糖（LPS）诱导的关节炎的炎症和关节破坏，以确定该细胞因子在炎性关节炎中的作用。设计：在mif缺陷小鼠和野生型小鼠中诱导抗cii Ab/ lps诱导的关节炎。同时评价抗mif多克隆抗体对抗cii抗体诱导的关节炎的影响。结果：抗cii Ab/ lps诱导的关节炎关节组织中MIF蛋白和mRNA表达明显增加。与野生型小鼠相比，抗cii Ab/ lps诱导的关节炎引起的滑膜炎症的组织病理学关节炎评分在抗mif Ab处理小鼠和mif缺陷小鼠中显著降低。此外，与野生型对照小鼠相比，mmp -缺陷小鼠抗cii Ab/ lps诱导的关节炎关节组织中MMP-13和mmp -2 mRNA水平显著降低。结论：这些结果表明，MIF在抗cii Ab/ lps诱导的小鼠关节炎模型中，在炎症和关节破坏中起关键作用，部分原因是通过诱导MMP-13和中性粒细胞浸润（通过诱导mmp -2）。(C) 2004 Elsevier Ltd.版权所有。
Objective: Previous studies have demonstrated that neutralization of macrophage migration inhibitory factor (MIF) by anti-MIF antibody decreases joint destruction in the collagen-induced arthritis model. The present study was undertaken to investigate whether selective deletion of MIF inhibits inflammation and joint destruction of the anti-type II collagen antibody (anti-CII Ab)/ lipopolysaccharide (LPS)-induced arthritis in mice, in order to determine the role of this cytokine in inflammatory arthritis.Design: Anti-CII Ab/LPS-induced arthritis was induced in MIF-deficient and wild-type mice. The effects of anti-MIF polyclonal antibody administration on anti-CII Ab-induced arthritis were also evaluated.Results: The expression of MIF protein and mRNA was induced in anti-CII Ab/LPS-induced arthritis joint tissues. Histopathological arthritis scores for synovial inflammation induced by anti-CII Ab/LPS-induced arthritis were significantly decreased in anti-MIF Ab-treated mice and in MIF-deficient mice compared to wild-type mice. In addition, mRNA levels of MMP-13 and MIP-2 in anti-CII Ab/LPS-induced arthritis joint tissues were significantly reduced in MIF-deficient mice compared to wild-type control mice.Conclusions: These results indicate that MIF plays a critical role in inflammation and joint destruction in the anti-CII Ab/LPSinduced arthritis model in mice, in part via induction of MMP-13 and neutrophil infiltration through the induction of MIP-2. (C) 2004 Elsevier Ltd. All rights reserved.