INVESTIGADORES
GIMENEZ Guadalupe
congresos y reuniones científicas
Título:
Lipids from virulent and attenuated B. bovis induce differential TLR2–mediated macrophage activation
Autor/es:
GIMENEZ G,; MAGALHÃES KG,; BELAUNZARÁN ML,; ECHAIDE I,; LAMMEL EM,; BOZZA P,; ISOLA ELD
Lugar:
Villa Carlos Paz, Córdoba,
Reunión:
Otro; XLIV Reunión de la Sociedad Argentina de Bioquímica y Biología Molecular.; 2008
Institución organizadora:
Sociedad Argentina de Bioquímica y Biología Molecular.
Resumen:
Babesia bovis, an intraerythrocytic apicomplexan protozoa of cattle, causes an acute infection with parasite persistence and its resolution depends on products of activated macrophages. In this sense, it has been demonstrated that the lipid fraction of B. bovis (mexican strain)-infected erythrocytes stimulates the production of nitric oxide (Brown WC, 2000). Herein, we report that the lipid fractions from B. bovis merozoites of R1A (attenuated) and S2P (pathogenic) strains induced higher TNFa and KC release in peritoneal macrophages (Mo) from wild type mice (WT) compared to unstimulated cells (ELISA). In contrast, this effect was inhibited in Mo from knock out toll like receptor 2 mice (KOTLR2). Moreover, the induction of lipid body formation (Osmium staining) in murine Mo by R1A and S2P lipids was significantly inhibited in TLR2-defective Mo when compared with WT cells. Interestingly, in both cases R1A lipids induced a significantly higher response than S2P. R1A lipids also induced the expression of Ciclooxigenase 2 (COX-2) in WT cells whereas this effect was not observed in KOTLR2 cells (Immunoblot). No COX-2 induction was detected in WT and KOTLR2 cells stimulated with S2P lipids. These results suggest that activation of Mo by B. bovis lipid fractions is mediated by TLR2 and the decreased inflammatory response observed with S2P lipids could be an immune modulation mechanism.