IHEM   20887
INSTITUTO DE HISTOLOGIA Y EMBRIOLOGIA DE MENDOZA DR. MARIO H. BURGOS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
RHOA SIGNALLING PATHWAY IN INVOLVED IN COXIELLA BURNETII PHAGOCYTOSIS
Autor/es:
SALINAS, R; AGUILERA, M; COLOMBO, M; LEYTON, L; BERÓN, W
Lugar:
Villa Carlos Paz, Córdoba
Reunión:
Congreso; XLIV Reunión Anual Sociedad Argentina de Investigaciones en Bioquímica y Biología Molecular; 2008
Institución organizadora:
Sociedad Argentina de Investigaciones en Bioquímicas y Biología Molecular
Resumen:
<!-- /* Style Definitions */ p.MsoNormal, li.MsoNormal, div.MsoNormal {mso-style-parent:""; margin-top:0cm; margin-right:0cm; margin-bottom:10.0pt; margin-left:18.0pt; text-align:justify; text-indent:12.0pt; line-height:200%; mso-pagination:widow-orphan; font-size:12.0pt; font-family:Arial; mso-fareast-font-family:"Times New Roman"; mso-ansi-language:ES-AR; mso-fareast-language:EN-US;} @page Section1 {size:612.0pt 792.0pt; margin:70.85pt 3.0cm 70.85pt 3.0cm; mso-header-margin:36.0pt; mso-footer-margin:36.0pt; mso-paper-source:0;} div.Section1 {page:Section1;} --> Phagocytosis is an important defense process against pathogens. This process is triggered by the interaction of pathogen ligands with host cell specific receptors such as CR3. The actin cytoskeleton is necessary for phagocytosis and Rho GTPases are well known regulators of actin dynamic. In particular, RhoA is mainly involved in CR3-dependent phagocytosis. On the other hand, it is known that Src and ROCK kinases are part of the Rho signalling pathway.  Coxiella burnetii (Cb) is an obligated intracellular pathogen that causes Q fever in humans. Cb phase II is an avirulent form that is phagocytosed through αVβ3 and CR3 receptors. Since Cb interacts with CR3, and RhoA is activated during CR3-mediated phagocytosis, we decide to analyze if Cb internalization induces RhoA activation in the host cell. Rho activation was measured using a RBD domain of Rhotekin, fused to GST,that recognizes Rho-GTP form and a pull-down assay. We observed that heat-killed Cb induced RhoA activation during HeLa cell infection. To assess the participation of Src and ROCK in Cb internalization, HeLa cells were incubated with PP2 or Y-27632, specific inhibitors of Src and ROCK, respectively, before infection. We observed that Cb internalization decreased significantly in the presence of both inhibitors. Al together, these results suggest that the RhoA, Src and ROCK are involving in heat-killed Cb phagocytosis