Monocyte chemoattractant protein-1 mRNA expression in the human burn wound.

The inflammatory response following a thermal insult begins with the skin itself. Langerhan's cells, tissue macrophages, keratinocytes, fibroblasts, and endothelial cells contribute to the initial events of wound healing with active and passive release of cell mediators. One of the mediators potentially important to the repair process is monocyte chemoattractant protein-1 (MCP-1). Macrophages, fibroblasts, endothelial cells, and keratinocytes can produce MCP-1 in response to inflammatory stimuli. Therefore, we evaluated 10 human burn wound specimens for MCP-1 mRNA using in situ hybridization. Selected specimens of different ages were examined using combined in situ hybridization and immunocytochemistry to identify cell types that expressed MCP-1 mRNA. Antibodies to HAM56 for macrophages, CD45 for bone marrow-derived cells, Factor VIII for endothelial cells, and Factor XIIIa for dermal antigen-presenting cells were included in these experiments. By Postburn Day 2, basal layer keratinocytes at the edges of the wound had upregulated MCP-1 message; the increased signal persisted in the rate pegs deep in the dermal wound bed through 49 days postinjury. Occasional FXIIIa+ immunostained dermal cells expressed MCP-1 mRNA. Islands of granulation tissue throughout the wound bed were positive for increased expression of MCP-1; endothelial cells and inflammatory cells both contributed to this upregulated signal. Our data support the theory that the skin itself is a component of the immune system and that noninflammatory cells contribute to the initiation and maintenance of the inflammation at a wound site. Failure to produce MCP-1 or other related mediators by indigenous cutaneous cells may delay the inflammatory response to injury and potentially disrupt other essential phases of wound repair.