Depletion of eosinophil infiltration by anti-IL-5 monoclonal antibody (TRFK-5) accelerates open skin wound epithelial closure.
Depletion of eosinophil infiltration by anti-IL-5 monoclonal antibody (TRFK-5) accelerates open skin wound epithelial closure.
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发表时间：
1997-09
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通讯作者：
James Yang;A. Torio;R. Donoff;G. Gallagher;Robert Egan;P. Weller;David T. W. Wong
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作者：
James Yang;A. Torio;R. Donoff;G. Gallagher;Robert Egan;P. Weller;David T. W. Wong
伤口愈合对物种在受伤后的生存至关重要。以仓鼠为实验模型，我们发现嗜酸性粒细胞显著渗入皮肤创面，并表达转化生长因子-α和-β1mRNAs和蛋白质。我们假设嗜酸性粒细胞在伤口愈合中很重要。由于没有一种动物模型的嗜酸性粒细胞存在遗传缺陷，检验这一假说的合适方法是选择性地减少和/或耗尽进入伤口部位的嗜酸性粒细胞。在这项研究中，我们报告了抗白介素5单抗(TRFK-5)治疗可以耗尽皮肤愈合伤口中的嗜酸性粒细胞。结果显示，实验组创面再上皮化愈合时间比对照组快4天(P<；0.01)。实验组第9天创面嗜酸性粒细胞密度明显低于对照组(P<；0.01)。在TRFK-5处理的每一只仓鼠中，伤口相关的嗜酸性粒细胞被耗尽到与未受伤的仓鼠皮肤相当的水平。这些结果表明，抗白介素5单抗治疗能有效地减少嗜酸性粒细胞在金黄地鼠皮肤愈合创面中的渗透，并提示嗜酸性粒细胞在负面影响创面再上皮化中的作用。
Wound healing is critical to the survival of the species after injury. Using hamsters as an experimental model, we have shown that eosinophils infiltrate prominently into skin wounds and that they express transforming growth factor-alpha and -beta 1 mRNAs and proteins. We hypothesized that eosinophils are important in wound healing. As no animal model is genetically deficient in eosinophils, a suitable way to test the hypothesis is to selectively reduce and/or deplete the influx of eosinophils into the wound sites. In this study, we report that anti-interleukin-5 monoclonal antibody (TRFK-5) treatment can deplete eosinophils in cutaneous healing wounds. We found that wound closure by re-epithelialization in the experimental group was 4 days faster than in the control group (P < 0.01). The density of eosinophils in day-9 wounds was significantly lower in the experimental group (P < 0.01). Wound-associated eosinophils in each of the TRFK-5-treated hamsters were depleted to the level comparable to unwounded hamster skin. These results demonstrate that anti-interleukin-5 monoclonal antibody treatment can effectively decrease eosinophil infiltration into hamster cutaneous healing wounds and indicate a role for eosinophils in negatively affecting wound re-epithelialization.