IHEM   20887
INSTITUTO DE HISTOLOGIA Y EMBRIOLOGIA DE MENDOZA DR. MARIO H. BURGOS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Autophagic activation by alpha-hemolysin from Staphylococcus aureus
Autor/es:
MARÍA BELÉN MESTRE; MARÍA ISABEL COLOMBO
Lugar:
Puerto Madryn, Chubut
Reunión:
Congreso; XLVI Reunión Anual de la SAIB; 2010
Institución organizadora:
SAIB
Resumen:
Staphylococcus aureus induces a caspase-independent cell death, with the participation of the autophagic pathway. Autophagy involves the sequestration of cytosolic components, organelles and microorganisms in a vacuole called autophagosome, which finally fuses with the lysosome to degrade the trapped material. We have recently shown that alpha-Hemolysin (Hla), a pore forming toxin, which is the main virulence factor secreted by S. aureus , is able to induce the autophagic pathway in CHO cells. The toxin caused a marked activation of autophagy in a concentration-dependent manner, as assessed by LC3-puncta formation. However, our results indicate that the LC3-positive vesicles generated in response to the toxin are not acidic and non-degradative compartments, suggesting that autophagosome maturation is inhibited by Hla. Interestingly, we have found that Hla-induced autophagy is independent of the PI3K/Beclin 1 complex, since the toxin effect was not prevented by silencing Beclin 1 or by the classical PI3K inhibitors 3-methyladenine and wortmannin. We have recently identified some of the essential molecules of the signaling pathway involved in this “non canonical” autophagic response induced by the toxin.