Effect of Glucocorticosteroid Treatment on Ovalbumin-Induced IgE-Mediated Immediate and Late Allergic Response in Guinea Pig

Abstract

The effect of glucocorticosteroid (GCS) treatment on ovalbumine-induced IgE-mediated immediate and late allergic response was studied in sensitized guinea pigs. The results show that the GCS budesonide (BUD) inhibits the allergen-induced IgE-mediated immediate and late bronchial obstruction. The effect on the early reaction is correlated to the inhibition of leukotrienes and histamine release. The importance of mediator release inhibition for the antianaphylactic effect of GCS is discussed. In examining the effect on the late reaction, it was found that BUD had to be present during the early reaction but did not inhibit the early reaction. Furthermore, the effect on the late reaction was correlated to the inhibition of vascular leakage but not to the infiltration of inflammatory cells as examined in bronchoalveolar lavage. The results indicate that some triggering factors important for the development of the late reaction are released during the early reaction. Inhibition of the release of that factor or the activation of inflammatory cells by that factor might be the mechanism behind the antiinflammatory activities of GCS.

Back to the future: re-establishing guinea pigin vivoasthma models

“…There are very few published studies in guinea pigs using the full power of broadband FOT, but based on published analyses there is every reason to believe that the respiratory system of the guinea pig will behave in a similar way as in any other laboratory animal [74]. Allergic guinea pigs display characteristic changes in AHR when exposed to methacholine with increases in Rn, G and H, commensurate with elevations in lung lavage eosinophils and neutrophils [83] supporting previous studies where glucocorticoids, xanthines, anti-histamines and β 2 adrenoceptor agonists have been shown to have positive effects on the guinea pig lung phenotype [84][85][86][87][88]. It is interesting to note that younger guinea pigs appear to be more sensitive to the sensitization allergen than older animals [89], suggesting that guinea pigs might be a model for age-dependent longitudinal studies.…”

Influence of sensitization and allergen provocation procedures on the development of allergen‐induced bronchial hyperreactivity in conscious, unrestrained guinea‐pigs

“…The failure of booster sensitization to induce BHR after the first allergen provocation was surprising, because using a booster has been claimed to increase BHR, 23'24 as well as IgE titres and the severity of the EAR. 25 It is possible that the 14 days between the last sensitization and the first allergen provocation was too short to enable sufficient IgE production. This is, however, unlikely since sensitivity to allergen is correlated with IgE titres, 15 and each animal in this group responded to the lowest allergen concentration applied.…”

Alpha-2-Macroglobulin-Kallikrein Complex: A Temperature-Sensitive Mediator in Contact-System-Induced Inflammation with a Potential Role in Late and Delayed Hypersensitivity Responses

“…It is known that the immedi ate reaction involves a release of mast cell or basophil mediators, and is commonly, but not necessarily, IgErelated [15][16][17], Late-phase reactions in humans may show peak activity between 6 and 8 h after the expo sure and residual activity up to 24 h, manifest evi dence of contact system activity and in contradistinc tion to the immediate reaction (except in the case of systemic anaphylaxis) can be blocked by the prior ad ministration of corticosteroids [18][19][20][21][22][23][24][25]. Delayed-type hypersensitivity, the best-known example being the classical tuberculin reaction, has been characterized as a complex expression of cellular immunity involv ing antigen-dependent changes in lymphocyte traffic, recruitment of lymphocytes without immunologic specificity and alterations in vascular permeability and blood flow [26].…”