MONOCYTE CHEMOATTRACTANT PROTEIN-1 MESSENGER-RNA EXPRESSION IN THE HUMAN BURN WOUND

Citation
Ns. Gibran et al., MONOCYTE CHEMOATTRACTANT PROTEIN-1 MESSENGER-RNA EXPRESSION IN THE HUMAN BURN WOUND, The Journal of surgical research, 70(1), 1997, pp. 1-6
Citations number
36
Categorie Soggetti
Surgery
ISSN journal
00224804
Volume
70
Issue
1
Year of publication
1997
Pages
1 - 6
Database
ISI
SICI code
0022-4804(1997)70:1<1:MCPMEI>2.0.ZU;2-V
Abstract
The inflammatory response following a thermal insult begins with the s kin itself. Langerhan's cells, tissue macrophages, keratinocytes, fibr oblasts, and endothelial cells contribute to the initial events of wou nd healing with active and passive release of cell mediators, One of t he mediators potentially important to the repair process is monocyte c hemoattractant protein-1 (MCP-1). Macrophages, fibroblasts, endothelia l cells, and keratinocytes can produce MCP-1 in response to inflammato ry stimuli. Therefore, we evaluated 10 human burn wound specimens for MCP-1 mRNA using in situ hybridization. Selected specimens of differen t ages were examined using combined in situ hybridization and immunocy tochemistry to identify cell. types that expressed MCP-1 mRNA. Antibod ies to HAM56 for macrophages, CD45 for bone marrow-derived cells, Fact or VDI for endothelial cells, and Factor XIIIa for dermal antigen-pres enting cells were included in these experiments. By Postburn Day 2, ba sal layer keratinocytes at the edges of the wound had upregulated MCP- 1 message; the increased signal persisted in the rete pegs deep in the dermal wound bed through 49 days postinjury. Occasional FXIIIa(+) imm unostained dermal cells expressed MCP-1 mRNA. Islands of granulation t issue throughout the wound bed were positive far increased expression of MCP-1; endothelial cells and inflammatory cells both contributed to this upregulated signal. Our data support the theory that the skin it self is a component of the immune system and that noninflammatory cell s contribute to the initiation and maintenance of the inflammation at a wound site. Failure to produce MCP-1 or other related mediators by i ndigenous cutaneous cells may delay the inflammatory response to injur y and potentially disrupt other essential phases of wound repair. (C) 1997 Academic Press.