Dehydroepiandrosterone suppresses eosinophil infiltration and airway hyperresponsiveness via modulation of chemokines and Th2 cytokines in ovalbumin-sensitized mice.

In this study, we evaluated the anti-inflammatory response and the mechanism by which dehydroepiandrosterone modulates immunity in ovalbumin-sensitized asthmatic mice. Female BALB/c mice were sensitized and challenged with ovalbumin and then treated with oral administration of dehydroepiandrosterone on days 21 to 27. The results showed dehydroepiandrosterone could suppress airway hyperresponsiveness and decrease eosinophil infiltration of the lungs in ovalbumin-sensitized mice. Moreover, dehydroepiandrosterone inhibited chemokines, including CCL11/eotaxin-1 and CCL24/eotaxin-2, and Th2-associated cytokine levels in bronchoalveolar lavage fluid. After the inflammatory human bronchial epithelial cell line BEAS-2B was treated with dehydroepiandrosterone, levels of proinflammatory cytokines and chemokines were inhibited, including IL-6, IL-8, CCL11, and CCL24. We suggested that dehydroepiandrosterone inhibited inflammation in bronchial epithelial cells as indicated by the suppression of Th2-associated cytokines and chemokines. Dehydroepiandrosterone also suppressed eosinophil migration and infiltration into the lung to improve the symptoms of asthma in ovalbumin-sensitized mice.