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In vitro activation of murine peritoneal macrophages by monocyte chemoattractant protein-1: upregulation of CD11b, production of proinflammatory cytokines, and the signal transduction pathway



In vitro activation of murine peritoneal macrophages by monocyte chemoattractant protein-1: upregulation of CD11b, production of proinflammatory cytokines, and the signal transduction pathway



Journal of Interferon and Cytokine Research 22(5): 527-538



The CC chemokine monocyte chemotactic protein-1 (MCP-1) is a major mediator of monocyte/macrophage infiltration at the inflammatory sides under both physiologic and pathologic conditions. We report the ability of MCP-1 to activate murine peritoneal macrophages in vitro for enhanced expression of CD11b, macrophage-mediated cytotoxicity, and production of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1). The macrophages treated with MCP-1 in vitro displayed significant cytolytic activity toward TNF-alpha-sensitive L929 cells in a dose-dependent manner. The macrophage-mediated L929 cytotoxicity was blocked in the presence of anti-TNF-alpha antibodies, suggesting the involvement of TNF-alpha. Production of TNF-alpha and IL-1 macrophages on MCP-1 treatment was maximum at 24 h of incubation with 100 ng/ml MCP-1. Enhanced TNF-alpha and IL-1beta mRNA expression was also demonstrated by RT-PCR, which revealed transcription of interferon gamma (IFN-gamma), IL-12, and related T cell-specific chemokine genes, KC and IP-10, in the MCP-1-treated macrophages. The pharmacologic inhibitors pertussis toxin (100 ng/ml), wortmannin (200 ng/ml), H-7 (10 microM), PD98059 (25 microM), and genistein (10 microg/ml) significantly inhibited TNF-alpha and IL-1 production in the MCP1-treated macrophages, suggesting the involvement of G-proteins, phosphoinositol-3-kinase (PI3K), protein kinase C, p42/44 MAPK, and tyrosine kinases in this process.

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Accession: 010811467

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PMID: 12060491

DOI: 10.1089/10799900252982007


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