Adrenal Steroids Modulate the Immune Response during Brucella abortus Infection by a Mechanism That Depends on the Regulation of Cytokine Production

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Abstract
Human brucellosis is a protean disease with a diversity of clinical signs and symptoms resulting from infection with Brucella species. Recent reports suggest a cross-regulation between adrenal steroids (cortisol and dehydroepiandroesterone, DHEA) and the immune system. Monocytes and macrophages are the main replication niche for Brucella. Therefore, we investigated the role of adrenal hormones on the modulation of the immune response mediated by macrophages in B. abortus infection. Cortisol treatment during B. abortus infection significantly inhibits cytokine, chemokine and MMP-9 secretion. In contrast, DHEA treatment had no effect. However, DHEA treatment increases the expression of coestimulatory molecules (CD40, CD86), the adhesion molecule CD54 and MHC-I and MHC-II expression on the surface of B. abortus infected monocytes. It is known that B. abortus infection inhibits MHC-I and MHC-II expression induced by IFN-γ treatment. DHEA reverses B. abortus down modulation of the MHC-I and II expression induced by IFN-γ. Taken together our data indicate that DHEA immune intervention may positively affect monocyte activity during B. abortus infection.

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