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通过腹腔注射巨噬细胞炎性蛋白-1α诱导小鼠腹腔巨噬细胞集落形成细胞

Induction of murine peritoneal macrophage colony-forming cells by peritoneal administration of macrophage inflammatory protein-1 alpha.

作者信息

Chen B, Chou T H, Sensenbrenner L

机构信息

Department of Internal Medicine, Wayne State University School of Medicine, Detroit, MI 48201.

出版信息

Exp Hematol. 1993 Nov;21(12):1591-6.

PMID:8405240
Abstract

Peritoneal injection of thioglycollate medium (TM) to mice results in a dramatic increase in total number of peritoneal macrophages within 48 to 72 hours. Unlike resident macrophages, a fraction (10 to 20%) of these newly arrived young macrophages, designated as macrophage colony-forming cells (M-CFC), are highly proliferative and formed macrophage colonies in vitro in the presence of either macrophage or granulocyte-macrophage colony-stimulating factor (M-CSF or GM-CSF). Using a reverse transcriptase polymerase chain reaction (RT-PCR) technique, peritoneal exudate macrophages (PEM) obtained 2 to 5 days after a single TM injection actively expressed mRNA for recombinant murine macrophage inflammatory protein-1 alpha (rmMIP-1 alpha). Yet none or only a trace amount of mRNA for MIP-1 alpha was detected in normal resident macrophages or PEM obtained 7 days after TM treatment. The effect of rmMIP-1 alpha on the induction of exudate M-CFC was investigated. Multiple intraperitoneal (IP) administration of rmMIP-1 alpha caused a marked increase in the total number of peritoneal M-CFC and macrophages similar to but weaker than the increase in TM-injected mice. The total number of neutrophils, mast cells, and eosinophils also increased, but with different kinetics, following multiple injections of rmMIP-1 alpha. rmMIP-1 alpha alone did not stimulate the proliferation of M-CFC, nor did it potentiate their responsiveness to either rmGM-CSF or recombinant human (rh) M-CSF in vitro. Taken together, our results suggest that MIP-1 alpha released by exudate macrophages is a major chemoattractant responsible for the migration of M-CFC from the circulation to the peritoneal cavity during a TM-induced inflammatory response.

摘要

向小鼠腹腔注射巯基乙酸盐培养基(TM)会导致在48至72小时内腹腔巨噬细胞总数急剧增加。与常驻巨噬细胞不同,这些新到达的年轻巨噬细胞中有一部分(10%至20%),被指定为巨噬细胞集落形成细胞(M-CFC),具有高度增殖性,并在巨噬细胞或粒细胞-巨噬细胞集落刺激因子(M-CSF或GM-CSF)存在的情况下在体外形成巨噬细胞集落。使用逆转录酶聚合酶链反应(RT-PCR)技术,在单次注射TM后2至5天获得的腹腔渗出巨噬细胞(PEM)可积极表达重组鼠巨噬细胞炎性蛋白-1α(rmMIP-1α)的mRNA。然而,在正常常驻巨噬细胞或TM处理7天后获得的PEM中未检测到或仅检测到微量的MIP-1α mRNA。研究了rmMIP-1α对渗出液M-CFC诱导的影响。多次腹腔内(IP)给予rmMIP-1α导致腹腔M-CFC和巨噬细胞总数显著增加,与注射TM的小鼠相似但较弱。多次注射rmMIP-1α后,中性粒细胞、肥大细胞和嗜酸性粒细胞的总数也增加,但动力学不同。单独的rmMIP-1α不会刺激M-CFC的增殖,在体外也不会增强它们对rmGM-CSF或重组人(rh)M-CSF的反应性。综上所述,我们的结果表明,渗出巨噬细胞释放的MIP-1α是一种主要的趋化因子,负责在TM诱导的炎症反应期间M-CFC从循环系统迁移到腹腔。

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Inflammation. 2002 Dec;26(6):259-71. doi: 10.1023/a:1021408500630.
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Effect of intraperitoneally administered recombinant murine granulocyte-macrophage colony-stimulating factor (rmGM-CSF) on the cytotoxic potential of murine peritoneal cells.腹腔注射重组鼠粒细胞-巨噬细胞集落刺激因子(rmGM-CSF)对鼠腹腔细胞细胞毒性潜能的影响。
Br J Cancer. 1999 Jan;79(1):89-94. doi: 10.1038/sj.bjc.6690016.
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The CC chemokine MIP-1alpha induces a selective monocyte infiltration following intradermal injection into nonhuman primates.
Inflammation. 1999 Feb;23(1):75-86. doi: 10.1023/a:1020243701890.