Expression and regulation of macrophage inflammatory protein-1 alpha by murine alveolar and peritoneal macrophages.
Expression and regulation of macrophage inflammatory protein-1 alpha by murine alveolar and peritoneal macrophages.
复制标题
DOI：
10.1165/ajrcmb.10.1.8292385
复制
发表时间：
1994
影响因子：
6.4
通讯作者：
G. M. VanOtteren;T. Standiford;S. Kunkel;J. Danforth;M. Burdick;L. Abruzzo;R. Strieter
中科院分区：
文献类型：
--
作者：
G. M. VanOtteren;T. Standiford;S. Kunkel;J. Danforth;M. Burdick;L. Abruzzo;R. Strieter
许多疾病状态的特点是炎症细胞在组织损伤部位聚集。单核巨噬细胞(M Phi)是炎症的关键细胞介质，通过产生调节性和趋化性细胞因子。巨噬细胞炎性蛋白-1α(MIP-1α)就是这样一种细胞因子，已被证明是小鼠巨噬细胞系(RAW 264.7)表达的主要可诱导趋化因子之一。我们推测MIP-1α是一种主要的单核细胞趋化因子，这种趋化因子的产生可能取决于所研究的M phi的特定群体。为了验证这一假设，我们分别通过支气管肺泡灌洗和腹膜灌洗分离了CD-1小鼠的肺泡巨噬细胞(AM Phi)和腹膜巨噬细胞(PM Phi)。棋盘分析表明，重组小鼠MIP-1α具有显著的中性粒细胞趋化活性，而不是趋化活性。特异性兔抗鼠MIP-1α血清可显著中和脂多糖刺激的AM Phi来源的单核细胞趋化活性(MCA)。相反，PM Phi来源的条件培养液不能产生可归因于MIP-1α的MCA。然后从AM Phi和PM Phi两个方面表征MIP-1α的产生。未受刺激的AM Phi和PM Phi不表达MIP-1αmRNA，而内毒素刺激的AM Phi和PM Phi均以时间依赖的方式表达MIP-1αmRNA。
A number of disease states are characterized by the accumulation of inflammatory cells at the site of tissue injury. Mononuclear phagocytes (M phi) represent key cellular mediators of inflammation via the production of regulatory and chemokinetic cytokines. One such cytokine, macrophage inflammatory protein-1 alpha (MIP-1 alpha), has been shown to be one of the major inducible chemotaxins expressed from murine macrophage cell lines (RAW 264.7). We postulated that MIP-1 alpha is a major monocyte chemoattractant produced by resident M phi, and the magnitude of production of this chemotaxin may depend upon the specific population of M phi studied. To test this hypothesis, we isolated alveolar macrophages (AM phi) and peritoneal macrophages (PM phi) from CD-1 mice by bronchoalveolar and peritoneal lavage, respectively. Recombinant murine MIP-1 alpha accounted for significant neutrophil chemokinetic rather than chemotactic activity, as assessed by checkerboard analysis. LPS-stimulated AM phi-derived monocyte chemotactic activity (MCA) was significantly neutralized by specific rabbit anti-murine MIP-1 alpha serum. In contrast, PM phi-derived conditioned media failed to produce MCA attributable to MIP-1 alpha. The production of MIP-1 alpha was then characterized from both AM phi and PM phi. While unstimulated AM phi and PM phi failed to express MIP-1 alpha mRNA, both AM phi and PM phi challenged with lipopolysaccharide (LPS) expressed MIP-1 alpha mRNA in a time-dependent fashion.(ABSTRACT TRUNCATED AT 250 WORDS)