氧自由基、细胞因子、黏附分子与肺损伤。
Oxygen radicals, cytokines, adhesion molecules, and lung injury.
作者信息
Ward P A
机构信息
Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602.
出版信息
Environ Health Perspect. 1994 Dec;102 Suppl 10(Suppl 10):13-6. doi: 10.1289/ehp.94102s1013.
Inflammatory injury in the lung or dermis occurring after systemic activation of complement or after local deposition of immune complexes is related to local activation of tissue macrophages and/or recruitment of blood neutrophils. While requirements for cytokines (IL-1, TNF alpha, MCP-1) vary with the model of injury, requirements for adhesion molecules (beta 2 integrins, selectins, ICAM-1) differ. In most cases the immediate events related to tissue injury can be linked to toxic products from oxygen and L-arginine. Whether there is a single toxic product or a variety of toxic products remains to be determined. These data emphasize similarities and differences in the mechanisms of inflammatory injury, as a function of the inciting inflammatory agent and the organ system involved.
补体系统全身性激活后或免疫复合物局部沉积后发生的肺部或真皮炎症损伤，与组织巨噬细胞的局部激活和/或血液中性粒细胞的募集有关。虽然细胞因子（白细胞介素-1、肿瘤坏死因子α、单核细胞趋化蛋白-1）的需求因损伤模型而异，但黏附分子（β2整合素、选择素、细胞间黏附分子-1）的需求则有所不同。在大多数情况下，与组织损伤相关的即刻事件可与来自氧和L-精氨酸的毒性产物联系起来。是否存在单一毒性产物或多种毒性产物仍有待确定。这些数据强调了炎症损伤机制中的异同，这取决于引发炎症的因子和所涉及的器官系统。
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