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Recent reports suggest a cross-regulation between adrenal steroids (cortisol and dehydroepiandrosterone [DHEA]) and the immune system. Monocytes and macrophages are the main replication niche for<jats:named-content content-type=\"genus-species\">Brucella<\/jats:named-content>. Therefore, we investigated the role of adrenal hormones on the modulation of the immune response mediated by macrophages in<jats:named-content content-type=\"genus-species\">B. abortus<\/jats:named-content>infection. Cortisol treatment during<jats:named-content content-type=\"genus-species\">B. abortus<\/jats:named-content>infection significantly inhibits cytokine, chemokine, and MMP-9 secretion. In contrast, DHEA treatment had no effect. However, DHEA treatment increases the expression of costimulatory molecules (CD40, CD86), the adhesion molecule CD54, and major histocompatibility complex class I (MHC-I) and MHC-II expression on the surface of<jats:named-content content-type=\"genus-species\">B. abortus<\/jats:named-content>-infected monocytes. It is known that<jats:named-content content-type=\"genus-species\">B. abortus<\/jats:named-content>infection inhibits MHC-I and MHC-II expression induced by gamma interferon (IFN-\u03b3) treatment. DHEA reverses<jats:named-content content-type=\"genus-species\">B. abortus<\/jats:named-content>downmodulation of the MHC-I and -II expression induced by IFN-\u03b3. 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