Expression of monocyte chemoattractant protein 1 (MCP-1) in vivo
Date
1994
DOI
Authors
Yu, Xiaohui
Version
OA Version
Citation
Abstract
Monocytes/macrophages play important roles in the initial response in tissue injuries, cell-mediated immune response and host defense to foreign insults such as bacteria and toxins. The infiltration of mononuclear cells is a common feature of many forms of chronic cell-mediated inflammatory responses and delayed type hypersensitivity reactions. Monocyte chemoattractant protein 1 (MCP-1) is a well-defined member of the chemokine family of proinflammatory cytokines. A variety of cells have been shown to secrete MCP-1 in vitro. The expression of MCP-1 in diseases with a chronic inflammatory component (characterized by mononuclear cell infiltration) in vivo has not been as well described. In the present study, the hypothesis that MCP-1 expression is specifically associated with three disease states featured by monocytic cellular infiltration (atherosclerosis, bacteria-induced gingival inflammation and skin delayed type hypersensitivity reaction) was tested. We tested the hypothesis that MCP-1 is differentially expressed in (1) blood vessels of hypercholesterolemic primates as compared with blood vessels from primates with normal blood cholesterol levels; (2) inflammatory gingival tissue as compared with normal gingival tissue; and (3) skin tissue with delayed type hypersensitivity reactions as compared with normal skin. We found that MCP-1 was produced in all the three diseases. The cell types expressing MCP-1 varied according to different tissue injuries and patogens. Cells secreting MCP-1 included both the normal resident cells such as smooth muscle cells (atherosclerosis), endothelial cells (gingival inflammation and dermatoses), fibroblasts (gingival inflammation) as well as the recruited monocytes/macrophages (in three diseases). In the primate model of hypercholesterolemia, we found that MCP-1 was expressed at both the protein and mRNA levels. In bacteria-induced gingival inflammation, MCP-1 was also detected at both the protein and mRNA levels. Quantitative analysis revealed that the numbers of MCP-1 expressing monocytes and blood vessels were directly related to the degree of inflammation. The distribution of MCP-1 expressing gingival fibroblasts and macrophages also varied with the degree of inflammation. In delayed type hypersensitivity reactions in the skin, MCP-1 expression was also detected. The cell types expressing MCP-1 and the patterns of MCP-1 expression observed for several inflammatory dermatoses were similar. Our finding that MCP-1 is produced in these three disease states with chronic inflammation as a feature suggests that MCP-1 is an important mediator for monocyte recruitment and amplification of inflammatory signals in such diseases.
Description
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Thesis (D.Sc.D.)--Boston University, Henry M. Goldman School of Graduate Dentistry, 1994.
Includes bibliographical references.
Thesis (D.Sc.D.)--Boston University, Henry M. Goldman School of Graduate Dentistry, 1994.
Includes bibliographical references.
License
This work is protected by copyright. Downloading is restricted to the BU community. If you are the author of this work and would like to make it publicly available, please contact open-help@bu.edu.