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Wound Repair Regen. 2001 Jan-Feb;9(1):28-33.

Modulation of macrophage recruitment into wounds by monocyte chemoattractant protein-1.

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  • 1Burn and Shock Trauma Institute, Department of Surgery, Loyola University Medical Center, Maywood, Illinois 60153, USA.


Previous studies suggest that normal wound repair requires the regulated production of monocyte and macrophage chemoattractants. The current study examines the role of monocyte chemoattractant protein-1 (MCP-1) in coordinating monocyte recruitment into sites of injury. MCP-1 protein was detected in both incisional and excisional murine wounds, with a peak concentration occurring slightly before maximum macrophage infiltration. Compared to wounds treated with control antibody, wounds treated with a neutralizing monoclonal anti-MCP-1 antibody contained significantly fewer macrophages (8.2 +/- 0.9 vs. 14 +/- 1.7 macrophages per high power field, p < 0.05). Conversely, the addition of recombinant MCP-1 to wounds resulted in a substantial increase in the number of macrophages (107% to 124% increase over untreated wounds, p < 0.01). Because macrophages promote wound healing, the effect of recombinant MCP-1 on the wound healing process was examined. Incisional wounds (n = 12) were either left untreated or treated with vehicle alone, 5 ng recombinant MCP-1 in vehicle, or 50 ng recombinant MCP-1 in vehicle. Wound disruption strength was determined on days 7, 14, 21, and 28 for each group. Wounds treated with MCP-1 exhibited a slight increase in wound disruption strength at nearly all time points but this increase did not reach statistical significance. Addition of 100 ng of MCP-1 to excisional wounds did not have any significant effect on wound reepithelialization. Taken together, the results show that MCP-1 is produced within wounds at physiologic concentrations, and is an important positive regulator of macrophage recruitment into sites of injury. Addition of exogenous MCP-1 to wounds of normal mice yields only modest enhancement of the repair process.

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