Modulation of macrophage recruitment into wounds by monocyte chemoattractant protein-1
Modulation of macrophage recruitment into wounds by monocyte chemoattractant protein-1
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DOI：
10.1046/j.1524-475x.2001.00028.x
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发表时间：
2001-01-01
影响因子：
2.9
通讯作者：
Gamelli, RL
中科院分区：
文献类型：
--
作者：
DiPietro, LA;Reintjes, MG;Gamelli, RL
以前的研究表明，正常的伤口修复需要单核细胞和巨噬细胞趋化因子的调节生产。目前的研究探讨了单核细胞趋化蛋白-1（MCP-1）在协调单核细胞募集到损伤部位中的作用。MCP-1蛋白在切口和切除的小鼠伤口中均被检测到，在最大巨噬细胞浸润之前出现峰值浓度。与用对照抗体处理的伤口相比，用中和性单克隆抗MCP-1抗体处理的伤口含有显著更少的巨噬细胞（8.2 +/-0.9对比14 +/-1.7巨噬细胞/高倍视野，p < 0.05）。相反，向伤口中加入重组MCP-1导致巨噬细胞数量的显著增加（与未处理的伤口相比增加107%至124%，p < 0.01）。由于巨噬细胞促进伤口愈合，因此检查了重组MCP-1对伤口愈合过程的影响。切口伤口（n = 12）不处理或用单独的媒介物、媒介物中的5 ng重组MCP-1或媒介物中的50 ng重组MCP-1处理。在第7、14、21和28天测定每组的伤口破裂强度。用MCP-1处理的伤口在几乎所有时间点都表现出伤口破裂强度的轻微增加，但这种增加没有达到统计学显著性。在切除伤口中加入100 ng MCP-1对伤口上皮再生没有任何显著影响。总之，结果表明，MCP-1在伤口内以生理浓度产生，并且是巨噬细胞募集到损伤部位的重要正调节剂。向正常小鼠的伤口中添加外源性MCP-1仅产生适度的修复过程增强。
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-l 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 ail 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.