á-hemolysin is required for the activation of the autophagic pathway in Staphylococcus aureusinfected cells

MARÍA BELÉN MESTRE; CLAUDIO M. FADER; CLAUDIA SOLA; MARÍA ISABEL COLOMBO1

AUTOPHAGY

LANDES BIOSCIENCE

Lugar: Austin, Texas; Año: 2010 vol. 6 p. 110 - 110

1554-8627

taphylococcus aureus is a pathogen that causes serious infectious diseases eventually leading to septic and toxic shock. Classically S. aureus has been considered an extracellular pathogen, but cumulative evidence indicates that it invades cells and replicates intracellularly leading to staphylococcal persistence and chronic disease. It has been previously shown that this pathogen localizes to LC3-labeled compartments and subverts the autophagy pathway. One of the key features of S. aureus infection is the production of a series of virulence factors, including secreted enzymes and toxins. In the present report we present evidence that the pore-forming toxin alpha-hemolysin (Hla) is a S. aureus secreted factor which participates in the activation of the autophagic pathway. In addition, our results indicate that although the toxin elicits an autophagic response this pathway is dysfunctional as indicated by the accumulation of the LC3-II form in cell lysates obtained from intoxicated cel