title: Studies on the mechanisms involved in antigen-evoked pleural inflammation in rats: contribution of IgE and complement.
abstract: Immunoglobulin E (IgE) has been shown to play a critical role in the allergic late-phase reaction, which is marked by intense leukocyte infiltration and edema. In this study we assessed the allergic pleural inflammation triggered by intrapleural (i.pl.) challenge in sensitized rats. We examined pleural effluent from actively sensitized rats following anti-IgE monoclonal antibody (mAb) (MARE-1) provocation for protein exudation, neutrophil as well as eosinophil accumulation. Inflammatory changes triggered by antigen after passive sensitization with IgE mAb was also assessed for comparison. Total serum level of IgE was found to be about threefold increased 7-8 days post-active sensitization, remaining augmented for at least 30 days. Increased levels of peritoneal leukocyte-bound IgE and serum IgE with specificity to ovalbumin were also detected. Nevertheless, the anti-IgE challenge in 14-day actively sensitized was shown to be a weak stimulus of neutrophil and eosinophil accumulation, despite being able to cause intense protein extravasation. Similarly, antigen challenge of IgE-passively sensitized rats caused protein leakage that was comparable to that induced by anti-IgE mAb in actively sensitized rats but led to a much lower neutrophil/eosinophil infiltration. Also, blockade of complement with recombinant human soluble C receptor-1 (sCR1) treatment prevented actively sensitized rats from reacting to antigen with neutrophil and eosinophil recruitment without modifying protein extravasation. These data suggest that IgE and complement-mediated mechanisms probably account for the exudation and leukocyte infiltration that is characteristic of the pleural inflammatory response observed in actively sensitized rats.
authors.affiliation: Instituto Oswaldo Cruz/IOC-FIOCRUZ, Rio de Janeiro, Brazil.
authors.forename: M C
authors.initials: MC
authors.lastname: Lima
authors.forename: A
authors.initials: A
authors.lastname: Prouvost-Danon
authors.forename: P M
authors.initials: PM
authors.lastname: e Silva
authors.forename: M S
authors.initials: MS
authors.lastname: Chagas
authors.forename: A S
authors.initials: AS
authors.lastname: Calheiros
authors.forename: R S
authors.initials: RS
authors.lastname: Cordeiro
authors.forename: D
authors.initials: D
authors.lastname: Latine
authors.forename: H
authors.initials: H
authors.lastname: Bazin
authors.forename: U S
authors.initials: US
authors.lastname: Ryan
authors.forename: M A
authors.initials: MA
authors.lastname: Martins
mesh_terms: D000077410:Aluminum Chloride; D017607:Aluminum Compounds; D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology; D002712:Chlorides; D004804:Eosinophils / Q000187:drug effects; D005260:Female; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology*; D007958:Leukocyte Count / Q000187:drug effects; D008297:Male; D009504:Neutrophils / Q000187:drug effects; D010047:Ovalbumin / Q000276:immunology; D010998:Pleurisy / Q000276:immunology*; D011506:Proteins / Q000276:immunology* / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011951:Receptors, Complement / Q000276:immunology
chemical_list: D017607:Aluminum Compounds; D000911:Antibodies, Monoclonal; D002712:Chlorides; D011506:Proteins; D011951:Receptors, Complement; D007073:Immunoglobulin E; D000077410:Aluminum Chloride; D010047:Ovalbumin