Inhalant corticosteroids inhibit hyperosmolarity-induced, and cooling and rewarming-induced interleukin-8 and RANTES production by human bronchial epithelial cells
S. Hashimoto et al., Inhalant corticosteroids inhibit hyperosmolarity-induced, and cooling and rewarming-induced interleukin-8 and RANTES production by human bronchial epithelial cells, AM J R CRIT, 162(3), 2000, pp. 1075-1080
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.