PAF and immune complex-induced injury

Abstract

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.