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Pleural fluid eosinophils suppress local IgE‐mediated protein exudation in rats
Author(s) -
BandeiraMelo Christianne,
Silva Patricia M.R. e,
Cordeiro Renato S.B.,
Martins Marco A.
Publication year - 1995
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.58.4.395
Subject(s) - neutrophilia , eosinophil , eosinophilia , pleural cavity , immunology , immunoglobulin e , microgram , pleurisy , medicine , lipopolysaccharide , eosinophilic , allergen , leukocytosis , allergy , pathology , biology , pleural effusion , asthma , antibody , surgery , biochemistry , in vitro
Eosinophils are supposed to play a critical role in the pathology of several allergic diseases because after activation they can release toxic and proinflammatory agents. In this study we have investigated whether IgE‐mediated rat pleurisy could be affected by an ongoing pleural eosinophilic inflammatory response. IgE‐passively sensitized rats were challenged with an intrapleural (i.pl.) injection of allergen (dinitrophenylated bovine serum albumin, 1 μg/cavity) and exudation assessed by measuring the amount of protein extravasated into the pleural cavity within 4 h. We have confirmed that lipopolysaccharide (LPS) stimulation (250 ng/cavity i.pl.) was followed by a marked pleural neutrophilia, apparent at 3 h, which was followed by an eosinophil accumulation noted within 48–72 h postchallenge. We have also confirmed that a boiled sample of LPS pleural washing (IPS‐PW, 200 μl i.pl.) caused selective eosinophilia in recipient rats. Pleural exudation remained unaltered when the allergenic challenge was performed 3 h after IPS in a condition of intense pleural fluid neutrophilia. In contrast, this was significantly reduced ( P < .001) when the challenge occurred 72 h after IPS or 24 h after IPS‐PW in selective pleural fluid eosinophilia. In another series of experiments repeated daily i.pl. injections of platelet‐activating factor (PAF; 1 μg/cavity) resulted in a progressive increase in eosinophil number recovered from the pleural cavity. The values were 1.2 ± 0.2, 3.0 ± 0.2, and 5.8 ± 0.5 × 10 6 eosinophils/cavity (mean±SEM) after 0, 1, and 4 injections, respectively. Allergen challenge performed after 0, 1, or 4 PAF stimulations led to pleural protein levels of 88.6 ± 5.7, 33.7 ± 0.7, and 19.4 ± 2.3 mg/cavity, respectively, indicating that the allergic pleurisy is inhibited in a manner dependent on the magnitude of eosinophil accumulation. Furthermore, the impairment of PAF‐induced eosinophil accumulation by cetirizine (30 mg/kg i.p.) restored the exudatory response. Exudation triggered by compound 48/80 (25 μg/cavity), histamine (200 μg/cavity), or 5‐hydroxytryptamine (100 μg/cavity) was not affected by four previous PAF daily injections. The findings indicate that allergen‐induced exudation is selectively down‐regulated in the eosinophil‐enriched pleural space of rats, a suppression that increased with increasing eosinophil number and disappeared after chemical impairment of the eosinophilia.