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Macrophage migration inhibitory factor induces phagocytosis of foreign particles by macrophages in autocrine and paracrine fashion.

机译:巨噬细胞迁移抑制因子诱导巨噬细胞以自分泌和旁分泌方式吞噬异物。

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摘要

Exposure to foreign particles sometimes causes inflammatory reactions through production of cytokines and chemoattractants by phagocytic cells. In this study, we focused on macrophage migration inhibitory factor (MIF) to evaluate its pathophysiological role in the phagocytic process. Immunohistochemical analysis of human pseudosynovial tissues retrieved at revision of total hip arthroplasty showed that infiltrating mononuclear and multinuclear cells were positively stained by both an anti-CD68 antibody and anti-human MIF antibody. For in vitro study, MIF was released from murine macrophage-like cells (RAW 264.7) in response to phagocytosis of fluorescent-latex beads in a particle dose-dependent manner. Northern blot analysis showed marked elevation of the MIF mRNA level in the phagocytic macrophage-like cells. Moreover, pretreatment of RAW 264.7 cells with rat recombinant MIF increased the extent of phagocytosis by 1.6-fold compared with the control. Taken together, these results suggest that MIF plays an important role by activating macrophages in autocrine and paracrine fashion to phagocytose foreign particles.
机译:暴露于外来颗粒有时会通过吞噬细胞产生细胞因子和趋化因子而引起炎症反应。在这项研究中,我们集中于巨噬细胞迁移抑制因子(MIF)来评估其在吞噬过程中的病理生理作用。对全髋关节置换术修复后取回的人假滑膜组织的免疫组织化学分析显示,抗CD68抗体和抗人MIF抗体均对浸润的单核细胞和多核细胞染色呈阳性。为了进行体外研究,响应于荧光胶乳珠的吞噬作用,以颗粒剂量依赖性方式从鼠巨噬细胞样细胞(RAW 264.7)释放MIF。 Northern印迹分析显示吞噬巨噬细胞样细胞中MIF mRNA水平显着升高。此外,与对照组相比,用大鼠重组MIF预处理RAW 264.7细胞可使吞噬作用的程度增加1.6倍。综上所述,这些结果表明,MIF通过以自分泌和旁分泌的方式激活巨噬细胞吞噬异源颗粒而发挥重要作用。

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