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Effects of long‐term oral treatment with leflunomide on allergic sensitization, lymphocyte activation, and airway inflammation in a rat model of asthma
Author(s) -
Torsten Uhlig,
David K. C. Cooper,
Ernst Eber,
Christine McMenamin,
Johannes H. Wildhaber,
Peter D. Sly
Publication year - 1998
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1046/j.1365-2222.1998.00309.x
Subject(s) - sensitization , leflunomide , ovalbumin , medicine , immunology , immunoglobulin e , eosinophil , allergic inflammation , bronchoalveolar lavage , antigen , allergy , asthma , rheumatoid arthritis , antibody , lung
Background Short‐term treatment with leflunomide is effective in suppressing antigen‐specific antibody production and allergen‐induced bronchoconstriction after sensitization. This agent may thus have a role in future primary prevention strategies in allergic disease. Objective The current study aimed to determine whether long‐term oral treatment with leflunomide prevents allergic sensitization permanently. Methods After sensitization with ovalbumin, six groups of rats ( n = 31) were treated daily with leflunomide or diluent for up to 30 days. Ovalbumin‐specific IgE and IgG were determined weekly for at least 2 weeks after cessation of treatment. T lymphocytes from another 21 animals were stimulated ex vivo with ovalbumin or concanavalin A. Results Ovalbumin‐specific IgE and IgG were lower during treatment with leflunomide compared with controls ( P < 0.002) but increased after the cessation of treatment. Antigen‐specific T‐cell proliferation was decreased in cells obtained from leflunomide treated animals ( P < 0.05), but not when stimulated with concanavalin A. Eosinophil ( P < 0.0001) and neutrophil ( P < 0.02) numbers in bronchoalveolar lavage 24 h after allergen challenge were lower in the leflunomide treated animals. Conclusions Leflunomide prevents antigen‐specific immunoglobulin production after sensitization during treatment, inhibits allergen‐induced airway inflammation and diminishes antigen‐specific T lymphocyte proliferation.