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. 1995 Jan;66(1):80-8.
doi: 10.1902/jop.1995.66.1.80.

Fibroblasts, mononuclear phagocytes, and endothelial cells express monocyte chemoattractant protein-1 (MCP-1) in inflamed human gingiva

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Fibroblasts, mononuclear phagocytes, and endothelial cells express monocyte chemoattractant protein-1 (MCP-1) in inflamed human gingiva

X Yu et al. J Periodontol. 1995 Jan.

Abstract

Gingival inflammation is initiated by bacterial colonization of the tooth surface. It is characterized by infiltration of mononuclear cells, a feature of many forms of chronic inflammation. Monocyte chemoattractant protein-1 (MCP-1) is the predominant monocyte chemoattractant secreted by a variety of cells in vitro. We examined MCP-1 expression in chronic gingival inflammation by double antibody immunohistochemistry that utilized rabbit anti-MCP-1 antibody simultaneously with mouse monoclonal antibodies to specific cellular markers. MCP-1 mRNA expression by fibroblasts in inflamed gingival tissues was examined by in situ hybridization. We report here that in human chronic gingival inflammation the principal cell type expressing MCP-1 in dense inflammatory infiltrates is the mononuclear phagocyte. The cells expressing MCP-1 in moderately inflamed areas and in adjacent areas to inflammatory infiltrates are mononuclear phagocytes and fibroblasts, while in areas of fibroblastic hyperplasia, MCP-1 positive cells are predominantly fibroblasts. We also demonstrate that in moderately and highly inflamed areas, the extent of MCP-1 expression is greater than that in adjacent normal/mildly inflamed areas. As the degree of inflammation increased, there is also a concomitant increase in the number of mononuclear phagocytes. Furthermore, it is apparent that most of the infiltrating monocytes/macrophages are positive for MCP-1 in vivo. Our finding that MCP-1 expression is unambiguously identified in fibroblasts suggests that they can play a role in host defense by initiating the recruitment of monocytes. In addition, the expression of chemokines such as MCP-1 may represent a mechanism for amplification of inflammatory signals in gingival inflammation.

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