INHIBITION OF AIRWAYS INFLAMMATION BY DEXAMETHASONE IS FOLLOWED BY REDUCED BRONCHIAL HYPERREACTIVITY IN BP2 MICE

Background Infiltration of inflammatory cells in the airways is a cons tant characteristic of asthma and is considered to result in bronchial hyperreactivity.(BHR). We have recently developed a model of BHR usin g a selection of mice, named BP2, which display eosinophil-dependent B HR following antigen challenges. An anti-IL-5 antibody suppressed anti gen-induced eosinophil recruitment to the airways and BHR in BP2 mice. Objective To investigate the implication of infiltrated inflammatory cells in the induction of BHR in mice. Methods The effects of glucocor ticosteroid dexamethasone on airways eosinophilia and BHR were observe d. Results Administration of dexamethasone at the dose of 1.25 mg/kg i .p. 1 h before each of four antigen provocations suppressed the airway s eosinophilia and BHR in response to intravenous 5-HT and to aerosoli zed methacholine, as well as IL-5 production in the BALF and in the se rum. By contrast, dexamethasone failed to reduce anaphylactic bronchoc onstriction. Conclusions These results suggest that dexamethasone exer ts its inhibitory effects on antigen-induced airways eosinophilia in m ice by inhibiting IL-5 production, but that it does not block the libe ration of anaphylactic mediators in mice.