Gibran N S, Ferguson M, Heimbach D M, Isik F F
Department of Surgery, University of Washington, Seattle 98104, USA.
J Surg Res. 1997 Jun;70(1):1-6. doi: 10.1006/jsre.1997.5017.
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.
热损伤后的炎症反应始于皮肤本身。朗格汉斯细胞、组织巨噬细胞、角质形成细胞、成纤维细胞和内皮细胞通过主动和被动释放细胞介质，参与伤口愈合的初始过程。对修复过程可能重要的介质之一是单核细胞趋化蛋白-1（MCP-1）。巨噬细胞、成纤维细胞、内皮细胞和角质形成细胞可响应炎症刺激产生MCP-1。因此，我们使用原位杂交技术评估了10份人类烧伤创面标本中的MCP-1 mRNA。使用原位杂交和免疫细胞化学相结合的方法，对不同年龄的选定标本进行检查，以确定表达MCP-1 mRNA的细胞类型。这些实验中包括针对巨噬细胞的HAM56抗体、针对骨髓来源细胞的CD45抗体、针对内皮细胞的因子VIII抗体和针对真皮抗原呈递细胞的因子XIIIa抗体。烧伤后第2天，伤口边缘的基底层角质形成细胞上调了MCP-1信息；在受伤后49天内，真皮伤口床深处的钉突中信号持续增加。偶尔有FXIIIa+免疫染色的真皮细胞表达MCP-1 mRNA。整个伤口床的肉芽组织岛MCP-1表达增加呈阳性；内皮细胞和炎症细胞均促成了这种上调信号。我们的数据支持以下理论：皮肤本身是免疫系统的一个组成部分，非炎症细胞有助于伤口部位炎症的启动和维持。局部皮肤细胞未能产生MCP-1或其他相关介质可能会延迟对损伤的炎症反应，并可能扰乱伤口修复的其他重要阶段。
