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Thymic atrophy caused by glucocorticoid excess is associated with infiltration by mononuclear phagocytes and epithelial cells undergoing apoptosis. Early events leading to the generation of apoptotic epithelial cells in atrophied thymus include the induction of the synthesis of various inflammatory cytokines and prostaglandins, most notably prostaglandin E2. Therefore, we tested the hypothesis that inhibition of prostaglandin synthesis in dexamethasone-treated mice leads to increased apoptosis of thymic epithelial cells and, thus, to the development of a thymic atrophy. Western immunoblotting and immunohistochemical staining revealed that thymuses from dexamethasone-treated mice showed increased expression of the inducible cyclooxygenase 2 (COX-2) and increased COX-2 enzymatic activity. Dexamethasone also caused an increase in the expression of inducible nitric oxide synthase. Immunocytochemical staining revealed that dexamethasone induced an increase in the number of cells undergoing apoptosis. Indomethacin, a specific inhibitor of COX-2, had a potent and sustained effect on the number of apoptotic cells in dexamethasone-treated mice. This effect of indomethacin was associated with an increase in

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