title: Inhalant corticosteroids inhibit hyperosmolarity-induced, and cooling and rewarming-induced interleukin-8 and RANTES production by human bronchial epithelial cells.
abstract: Inhaled corticosteroids are widely used for the treatment of bronchial asthma, and a long-term treatment with inhaled corticosteroids is effective in preventing exercise-induced bronchoconstriction (EIB). We have previously shown that hyperosmolarity, and cooling and rewarming induced interleukin-8 (IL-8) expression in human bronchial epithelial cells (BEC). However, the effect of inhalant corticosteroids on hyperosmolarity-induced, and cooling and 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 cooling and rewarming-induced IL-8 and RANTES production. Because our previous studies have shown that p38 mitogen-activated protein (MAP) kinase and c-Jun-NH(2)-terminal kinase (JNK) regulate hyperosmolarity-induced, and cooling and 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 BDP and BUD did not inhibit hyperosmolarity-induced and cooling-induced p38 MAP kinase and JNK activation. These results indicated that inhalant corticosteroids inhibited hyperosmolarity-, and cooling and rewarming-induced IL-8 and RANTES production; however, the mechanism of inhaled corticosteroid-mediated inhibition of hyperosmolarity-induced, and cooling and rewarming- induced cytokine production remains to be clarified.
authors.affiliation: First Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan. shuh@med.nihon-u.ac.jp
authors.forename: S
authors.initials: S
authors.lastname: Hashimoto
authors.forename: Y
authors.initials: Y
authors.lastname: Gon
authors.forename: K
authors.initials: K
authors.lastname: Matsumoto
authors.forename: I
authors.initials: I
authors.lastname: Takeshita
authors.forename: S
authors.initials: S
authors.lastname: Maruoka
authors.forename: T
authors.initials: T
authors.lastname: Horie
mesh_terms: D000280:Administration, Inhalation; D000287:Administration, Topical; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001250:Asthma, Exercise-Induced / Q000276:immunology; D001507:Beclomethasone / Q000494:pharmacology*; D001833:Body Temperature Regulation / Q000187:drug effects*; D001980:Bronchi / Q000187:drug effects* / Q000276:immunology; D019819:Budesonide / Q000494:pharmacology*; D002478:Cells, Cultured; D018946:Chemokine CCL5 / Q000378:metabolism*; D004847:Epithelial Cells / Q000187:drug effects* / Q000276:immunology; D005938:Glucocorticoids; D006801:Humans; D016209:Interleukin-8 / Q000378:metabolism*; D014882:Water-Electrolyte Balance / Q000187:drug effects*
chemical_list: D000893:Anti-Inflammatory Agents; D018946:Chemokine CCL5; D005938:Glucocorticoids; D016209:Interleukin-8; D019819:Budesonide; D001507:Beclomethasone