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Therefore, using a pharmacological inhibitor, celecoxib, we investigated the role of prostaglandins in host defense against<jats:italic>Histoplasma capsulatum<\/jats:italic>infection in C57BL\/6 mice. Our results showed that treatment with celecoxib inhibited cyclooxygenase 2, reduced the total fungal burden, and reduced the concentration of PGE<jats:sub>2<\/jats:sub>, cytokines, lymphocytes, neutrophils, and mononuclear cells in the bronchoalveolar space and lung parenchyma. In addition, celecoxib treatment increased the synthesis of nitric oxide, IFN-<jats:italic>\u03b3<\/jats:italic>, LTB<jats:sub>4<\/jats:sub>, and the phagocytic capacity of alveolar macrophages. Moreover, celecoxib treatment increased the survival of mice after infection with a lethal inoculum of<jats:italic>H. capsulatum<\/jats:italic>. These results suggest that prostaglandins alter the host immune response and play an important role in the pathogenesis of histoplasmosis. 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