Fibroblasts, mononuclear phagocytes, and endothelial cells express monocyte chemoattractant protein-1 (MCP-1) in inflamed human gingiva.
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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Department of Periodontology and Oral Biology, Boston University School of Graduate Dentistry, MA, USA.
Graves
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D000818:Animals; D000911:Antibodies, Monoclonal; D018932:Chemokine CCL2; D002630:Chemotactic Factors / Q000096:biosynthesis* / Q000276:immunology; D002634:Chemotaxis, Leukocyte; D002908:Chronic Disease; D016207:Cytokines / Q000096:biosynthesis; D016373:DNA, Antisense; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism; D005347:Fibroblasts / Q000276:immunology / Q000378:metabolism; D005891:Gingivitis / Q000276:immunology* / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D017403:In Situ Hybridization; D008264:Macrophages / Q000276:immunology / Q000378:metabolism; D051379:Mice; D009000:Monocytes / Q000276:immunology / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D011817:Rabbits
D000911:Antibodies, Monoclonal; D018932:Chemokine CCL2; D002630:Chemotactic Factors; D016207:Cytokines; D016373:DNA, Antisense; D012333:RNA, Messenger