Inhalant corticosteroids inhibit hyperosmolarity-induced, and cooling and rewarming-induced interleukin-8 and RANTES production by human bronchial epithelial cells

Inhaled corticosteroids are widely used for the treatment of bronchial asth ma, and a long-term treatment with inhaled corticosteroids is effective In preventing exercise-induced bronchoconstriction (EIB), We have previously s hown that hyperosmolarity, and cooling and rewarming induced interleukin-8 (IL-8) expression in human bronchial epithelial cells (BEC). However, the e ffect of inhalant corticosteroids on hyperosmolarity-induced, and cooling a nd rewarming-induced IL-8 and RANTES production has not been determined. To clarify these issues, we examined the effect of inhalant corticosteroids, beclomethasone dipropionate (BDP), and budesonide (BUD) on hyperosmolarity- induced, and cooling and rewarming-induced IL-8 and RANTES production. The results showed that BDP and BUD inhibited hyperosmolarity-induced, and cool ing and rewarming-induced IL-8 and RANTES production. Because our previous studies have shown that p38 mitogen-activated protein (MAP) kinase and c-Ju n-NH2-terminal kinase (JNK) regulate hyperosmolarity-induced, and cooling a nd rewarming-induced IL-8 and RANTES production, we examined the effect of BDP and BUD on p38 MAP kinase and JNK activation. The results showed that B DP and BUD did not inhibit hyperosmolarity-induced and cooling-induced p38 MAP kinase and JNK activation. These results indicated that inhalant cortic osteroids inhibited hypersomolarity-, and cooling and rewarming-induced IL- 8 and RANTES production; however, the mechanism of inhaled corticosteroid-m ediated inhibition of hyperosmolarity-induced, and cooling and rewarming-in duced cytokine production remains to be clarified.