Brucella abortus lipoproteins down-regulate the IFNg-induced expression of Class II MHC molecules in the human monocytic line THP1.

BARRIONUEVO P.; ASTRID ZWERDLING,; JULIANA CASSATARO,; KARINA PASQUEVICH,; GARCÍA SAMARTINO C.; GUILLERMO H. GIAMBARTOLOMEI

Córdoba

Congreso; VII Latin American Congress of Immunology.; 2005

Brucella abortus induces a potent Th1 response, yet is capable to modulate this response and to establish a chronic infection. We recently have demonstrated that lipoproteins, not lipopolysaccharide (LPS), are the key mediators of the pro-inflammatory response elicited by heat-killed Brucella abortus (HKBA). Here, we investigated the effect of Brucella abortus on the activation of human monocytes/macrophages by IFN-g. THP-1 cells were incubated for 48 h with IFN-g in the presence of HKBA, and the expression of MHC-II molecules were evaluated by flow cytometry. HKBA down-regulated the IFN-g-induced expression of MHC-II molecules in a dose-dependent fashion. Polimixin B, a specific inhibitor of LPS, had not effect on this response. In addition, the Brucella abortus LPS was unable to reduce the expression of MHC-II molecules induced by IFN-g. To investigate the role of Brucella lipoproteins in the down-regulation of MHC-II expression mediated by HKBA we used Omp 19 as a Brucella lipoprotein model. Lipidated (L)-Omp 19, but not its unlipidated form, induced the decrease of IFN-g-induced MHC-II expression in a dose-dependent fashion. Together, these results entail a mechanism whereby Brucella abortus may inhibit IFN-g-activation in monocytes/macrophages and to evade immune surveillance.