Monocyte chemoattractant protein-1 expression and monocyte recruitment in osseous inflammation

Date
1995
DOI
Authors
Rahimi, Pourang
Version
OA Version
Citation
Abstract
In bone, early events in inflammation involve production and release of primary pro-inflammatory cytokines such as IL-1[Beta]. By activation of target cells, these cytokines are thought to induce a second wave of cytokines including monocyte chemoattractant protein-1 (MCP-1). MCP-1 is a chemokine that specifically stimulates monocytes/macrophages and basophils. Experiments were undertaken to examine the expression of MCP-1 in bone associated cells both in vivo and in vitro. To observe in vivo expression of MCP-1, an inflammatory lesion was created in the murine mandible. Immunohistochemistry experiments utilizing specific antibodies to MCP- 1 were conducted to identify MCP-1 expressing cells in inflamed and non-inflamed bone. We found that osteoblasts were the principal cells expressing MCP-1 in inflamed bone. There was little or no MCP-1 expression in non-inflamed bone. Immunohistochemistry experiments were carried out to assess monocyte recruitment during osseous inflammation. The number of MCP-1 positive cells was significantly correlated to the number of monocytes/macrophages present (N=15, r = 0.69, p is [equal to or less than] 0.01). We next examined the ability of isolated bone cells to produce MCP-1 in response to IL-1[Beta] in vitro. Normal osteoblasts and osteoclasts were collected from murine long bones, and were incubated with IL-1[Beta]. Immunohistochemistry was carried out utilizing specific antibodies to MCP-1. Both osteoblasts and osteoclasts expressed MCP-1 when pre-incubated with IL-1[Beta], but did not express MCP-1 without IL-1[Beta] stimulation. These in vitro and in vivo results strongly suggest that MCP-1 is an important mediator involved in the recruitment of monocytes/macrophages in inflamed bone.
Description
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Thesis (M.Sc.D.)--Boston University. Henry M. Goldman School of Graduate Dentistry, 1995 (Orthodontics).
Includes bibliographic references (leaves 46-57).
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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.