BACKGROUND: Infiltration of inflammatory cells in the airways is a constant characteristic of asthma and is considered to result in bronchial hyperreactivity (BHR). We have recently developed a model of BHR using a selection of mice, named BP2, which display eosinophil-dependent BHR following antigen challenges. An anti-IL-5 antibody suppressed antigen-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 glucocorticosteroid dexamethasone on airways eosinophilia and BHR were observed. RESULTS: Administration of dexamethasone at the dose of 1.25 mg/kg i.p. 1 h before each of four antigen provocations suppressed the airways eosinophilia and BHR in response to intravenous 5-HT and to aerosolized methacholine, as well as IL-5 production in the BALF and in the serum. By contrast, dexamethasone failed to reduce anaphylactic bronchoconstriction. CONCLUSIONS: These results suggest that dexamethasone exerts its inhibitory effects on antigen-induced airways eosinophilia in mice by inhibiting IL-5 production, but that it does not block the liberation of anaphylactic mediators in mice.
BACKGROUND: Infiltration of inflammatory cells in the airways is a constant characteristic of asthma and is considered to result in bronchial hyperreactivity (BHR). We have recently developed a model of BHR using a selection of mice, named BP2, which display eosinophil-dependent BHR following antigen challenges. An anti-IL-5 antibody suppressed antigen-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 glucocorticosteroiddexamethasone on airways eosinophilia and BHR were observed. RESULTS: Administration of dexamethasone at the dose of 1.25 mg/kg i.p. 1 h before each of four antigen provocations suppressed the airways eosinophilia and BHR in response to intravenous 5-HT and to aerosolized methacholine, as well as IL-5 production in the BALF and in the serum. By contrast, dexamethasone failed to reduce anaphylactic bronchoconstriction. CONCLUSIONS: These results suggest that dexamethasone exerts its inhibitory effects on antigen-induced airways eosinophilia in mice by inhibiting IL-5 production, but that it does not block the liberation of anaphylactic mediators in mice.
Authors: Venkata R Narala; Rajesh Ranga; Monica R Smith; Aaron A Berlin; Theodore J Standiford; Nicholas W Lukacs; Raju C Reddy Journal: Respir Res Date: 2007-12-04