Abstract
The effect of live RSV, RSV antigen-antibody complexes, and antibody to RSV on oxidative functions of human PMN was determined by employing luminol-dependent-chemiluminescence (LDCL). The presence of immune complexes was established by Raji cell radioimmune assay (RIA) and by the presence of immune aggregates on electron microscopy. The fresh PMN were obtained from healthy adult volunteers. RSV or antibody to RSV alone failed to induce significant degree of LDCL. However, RSV and RSV antibody mixtures generated significant degree of LDCL (P<0.001). The degree of LDCL activity induced by the virus-antibody mixtures was directly proportional to the presence and concentration of RSV-specific immune complexes as detected by RIA and EM. Removal of immune complexes by ultracentrifugation effectively eliminated the LDCL responses. LDCL activity was reduced four-fold after complement depletion. These data suggest a marked activation of oxidative metabolic pathway of PMN by RSV specific immune complexes. It is proposed that PMN mobilized to respiratory epithelium during the course of RSV infection, rather than the respiratory epithelium itself may serve as the targets for immune complex deposition. Such interaction may mediate the pathogenesis of RSV infection and bronchospasm via the possible release of metabolic products such as prostaglandins or thromboxanes from activated PMN.
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