STUDIES ON THE MECHANISMS INVOLVED IN ANTIGEN-EVOKED PLEURAL INFLAMMATION IN RATS - CONTRIBUTION OF IGE AND COMPLEMENT

Immunoglobulin E (IgE) has been shown to play a critical role in the a llergic late-phase reaction, which is marked by intense leukocyte infi ltration and edema, In this study we assessed the allergic pleural inf lammation triggered by intrapleural (i.pl.) challenge in sensitized ra ts, We examined pleural effluent from actively sensitized rats followi ng anti-IgE monoclonal antibody (mAb) (MARE-1) provocation for protein exudation, neutrophil as well as eosinophil accumulation, Inflammator y changes triggered by antigen after passive sensitization with IgE mA b was also assessed for comparison, Total serum level of IgE was found to be about threefold increased 7-8 days post-active sensitization, r emaining augmented for at least 30 days, Increased levels of peritonea l leukocyte-bound IgE and serum IgE with specificity to ovalbumin were also detected, Nevertheless, the anti-IgE challenge in 14-day activel y sensitized was shown to be a weak stimulus of neutrophil and eosinop hil accumulation, despite being able to cause intense protein extravas ation. Similarly, antigen challenge of IgE-passively sensitized rats c aused protein leakage that was comparable to that induced by anti-IgE mAb in actively sensitized rats but led to a much lower neutrophil/eos inophil infiltration, Also, blockade of complement with recombinant hu man soluble C receptor-1 (sCR1) treatment prevented actively sensitize d rats from reacting to antigen with neutrophil and eosinophil recruit ment without modifying protein extravasation, These data suggest that IgE and complement-mediated mechanisms probably account for the exudat ion and leukocyte infiltration that is characteristic of the pleural i nflammatory response observed in actively sensitized rats.