Brucella abortus lipoproteins induce dendritic cell maturation.

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

Córdoba, Argentina

Congreso; VII Latin American Congress of Immunology.; 2005

ALAI

The adjuvant and carrier heat-killed Brucella abortus (HKBA) is a well-established Th1-promoting stimulus. We have recently demonstrated that Brucella abortus lipoproteins stimulate cells from the innate immune system and induced the secretion of pro-inflammatory cytokines. Here, we investigated the ability of these lipoproteins to induce DC maturation. HKBA induced DC maturation as assessed by the increased expression of CD83, CD80 and CD86. Polimixin B, an inhibitor of LPS activity, had no effect on HKBA-induced DC maturation. Brucella LPS was unable to induce DC maturation. To investigate the role of B. abortus lipoproteins in HKBA-induced DC maturation we used Omp19 as a Brucella lipoprotein model. Stimulation with Omp19 increased the expression of CD83, CD80 and CD86 in a dose dependent-fashion. In addition, Omp19-treated DC produced TNF-a, IL-10 and IL-6. The lipid moiety of Omp19 was shown to be essential for the induction of maturation, since unlipidated Omp19 was unable to induce DC maturation or cytokine release. These results demonstrate that B. abortus lipoproteins are likely to be the main triggers of HKBA-induced DC maturation and as such could be the key components of HKBA Th1 adjuvant activity. These findings may have important implications in the rational design of vaccines that could exploit the adjuvant properties of lipoproteins for enhancing DC-mediated induction of cellular immune responses.