Warren J S, Johnson K J, Ward P A
Department of Pathology, University of Michigan Medical School, Ann Arbor 48109.
J Lipid Mediat. 1990;2 Suppl:S229-37.
Acute immune complex-mediated dermal vasculitis and pulmonary alveolitis have been induced in rats by the intradermal injection or intrapulmonary instillation of rabbit polyclonal antibody to bovine serum albumin (BSA), followed by intravenous injection of antigen. In the dermis, using reconstitution experiments in neutrophil-depleted rats and platelet-activating factor (PAF) receptor antagonists, we have shown that accessibility of PAF receptors on neutrophils is required for the full expression of dermal vascular injury. In the lung, intratracheal instillation of PAF receptor antagonists (with anti-BSA) results in a 54% suppression of pulmonary vascular leakage, suggesting that PAF receptors are necessary for the full expression of injury. These data suggest that in immune complex-induced tissue damage in which neutrophils and their oxygen radicals and proteases play a key role, there is an interplay of PAF and neutrophils required for the full expression of injury. The possible mechanisms involved will be discussed.
通过皮内注射或肺内滴注兔抗牛血清白蛋白（BSA）多克隆抗体，随后静脉注射抗原，在大鼠中诱导出了急性免疫复合物介导的皮肤血管炎和肺泡炎。在真皮中，利用中性粒细胞减少的大鼠进行的重组实验以及血小板活化因子（PAF）受体拮抗剂，我们已经表明，中性粒细胞上PAF受体的可及性是真皮血管损伤充分表达所必需的。在肺中，气管内滴注PAF受体拮抗剂（与抗BSA一起）可使肺血管渗漏抑制54%，这表明PAF受体是损伤充分表达所必需的。这些数据表明，在免疫复合物诱导的组织损伤中，中性粒细胞及其氧自由基和蛋白酶起关键作用，损伤的充分表达需要PAF和中性粒细胞之间的相互作用。将讨论其中可能涉及的机制。
