B. abortus lipoproteins down-regulate the IFN-gamma-induced expression of class I MHC molecules in the human monocytic cell line THP-1

P. BARRIONUEVO; A. ZWERDLING; J. CASSATARO; K. PASQUEVICH; C. GARCIA SAMMARTINO; G.H. GIAMBARTOLOMEI

Córdoba, Argentina

Congreso; VII Congreso Latinoamericano de Inmunología; 2005

Brucella abortus induces a potent proinflammatory response, yet is capable to modulate this response and to establish chronic infection. We recently reported that lipoproteins, not lipopolysaccharide (LPS), are the key mediators of the proinflammatory response elicited by heat-killed Brucella abortus (HKBA).  Here, we investigate 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 (100 U/ml) and/or HKBA 108 to 1010 bacteria/ml and the expression of MHC-II molecules were evaluated by flow cytometry. The results demonstrate that HKBA down-regulate the IFN-g-induced expression of MHC-II molecules in a dose dependent-fashion. Polimixin B, a specific inhibitor of LPS activity, had not effect on HKBA-mediated IFN-g-induced MHC-II expression down-regulation. 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 HKBA-mediated IFN-g-induced MHC-II expression down-regulation we used Omp 19. Lipidated (L)-Omp 19, but not the unlipidated form, induced the decrease of IFN-g-induced expression of MHC-II in a dose-dependent fashion. Similar results with HKBA and L-Omp19 were obtained on IFN-g-induced expression of Fc receptors for IgG type I (FcgRI, CD64). Together, these results entail a mechanism whereby Brucella abortus may to inhibit IFN-g activation in monocytes/macrophages and to evade immune surveillance