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
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.