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巨噬细胞移动抑制因子以自分泌和旁分泌方式诱导巨噬细胞吞噬外来颗粒。

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

作者信息

Onodera S, Suzuki K, Matsuno T, Kaneda K, Takagi M, Nishihira J

机构信息

Department of Orthopaedic Surgery, Hokkaido University School of Medicine, Sapporo, Japan.

出版信息

Immunology. 1997 Sep;92(1):131-7. doi: 10.1046/j.1365-2567.1997.00311.x.

DOI:10.1046/j.1365-2567.1997.00311.x
PMID:9370935
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1363992/
Abstract

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.

摘要

接触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发炎症反应。在本研究中,我们聚焦于巨噬细胞迁移抑制因子(MIF),以评估其在吞噬过程中的病理生理作用。对全髋关节置换翻修时获取的人假性滑膜组织进行免疫组织化学分析显示,浸润的单核细胞和多核细胞被抗CD68抗体和抗人MIF抗体均呈阳性染色。在体外研究中,MIF以颗粒剂量依赖性方式从鼠巨噬细胞样细胞(RAW 264.7)中释放,这是对荧光乳胶珠吞噬的反应。Northern印迹分析显示,吞噬性巨噬细胞样细胞中MIF mRNA水平显著升高。此外,用大鼠重组MIF预处理RAW 264.7细胞,与对照组相比,吞噬程度增加了1.6倍。综上所述,这些结果表明,MIF通过以自分泌和旁分泌方式激活巨噬细胞来吞噬外来颗粒,发挥重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab62/1363992/03e1160cc007/immunology00049-0142-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab62/1363992/576bccd876b2/immunology00049-0141-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab62/1363992/085fc8072ff1/immunology00049-0142-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab62/1363992/03e1160cc007/immunology00049-0142-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab62/1363992/576bccd876b2/immunology00049-0141-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab62/1363992/085fc8072ff1/immunology00049-0142-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab62/1363992/03e1160cc007/immunology00049-0142-b.jpg

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