IHEM   20887
INSTITUTO DE HISTOLOGIA Y EMBRIOLOGIA DE MENDOZA DR. MARIO H. BURGOS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Intracellular pathogens and cell death.
Autor/es:
COLOMBO M.I.
Lugar:
São Paulo Brazil.
Reunión:
Simposio; ICDS Meeting "Signaling in cell death survival, proliferation and degeneration? June-10-13, 2011; 2011
Institución organizadora:
ICDS
Resumen:
Symposium: Regulation of Death in Disease  Abstract Title: Intracellular pathogens and cell death María I. Colombo- IHEM-CONICET- Facultad de Ciencias Médicas- Universidad Nacional de Cuyo- Mendoza-Argentina. Programmed cell death (PCD) is a common consequence upon bacterial or viral infections. This PCD is a component of the host defense system against invasive pathogens whereas, in other cases, is an element of the pathogen survival strategy. However, other microorganisms modulate diverse cell mechanisms to actually prevent the death of the host cell.  Pathogens secrete a series of virulence factors and toxins to modulate both survival and host cell death pathways. We have found that Coxiella burnetii modulates both autophagy and apoptotic pathways via Beclin 1/Bcl-2 interplay to establish a successful infection in the host cell. Indeed, Coxiella prevents apoptosis protecting the host cell to generate a persistent bacterial infection. Staphylococcus aureus also subverts the autophagy pathway and replicates intracellularly in LC3-labeled compartments. We have presented evidence that the pore-forming toxin a-hemolysin (Hla) is a S. aureus secreted factor necessary for the activation of the autophagic pathway. Interestingly, this pathogen leads to a toxin-dependent activation of autophagy which is independent of Beclin 1, suggesting the involvement of a non-canonical autophagy pathway. Understanding the subversion of the host machinery by microorganisms is an important task to get new insights into how infection takes place and progresses, and what is the final outcome of the infected cell.