Brucella abortus lipoproteins down-regulate the IFN-g-induced expression of class II MHC (MHC-II) molecules in the human monocytic cell line THP-1.

BARRIONUEVO, PAULA; ZWERDLING, ASTRID; CASSATARO, JULIANA; PASQUEVICH, KARINA; GARCÍA SAMARTINO, CLARA; GIAMBARTOLOMEI, GUILLERMO

Córdoba, Argentina.

Congreso; VII Congreso Latinoamericano de Inmunología (ALAI).; 2005

Asociación Latinoamericana de Inmunología (ALAI).

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.