Staphylococcus aureus promotes autophagy by decreasing intracellular cAMP levels. Autophagy. 2012 Oct 9;8(12).

MESTRE, M.B.; COLOMBO M.I.

AUTOPHAGY

LANDES BIOSCIENCE

Lugar: Austin, Texas; Año: 2012 vol. 8

1554-8627

Staphylococcus aureus is an intracellular bacterium responsible for several diseases in the human being. This pathogen escapes from the phagolysosomal pathway, increasing intracellular bacterial survival and killing the eukaryotic host cell. S. aureus is able to produce several virulence factors, including secreted enzymes and toxins. The main virulence factor of S. aureus, the pore-forming toxin a-hemolysin (Hla), is the secreted factor responsible for the activation of a non canonical autophagic pathway. We have recently demonstrated that cAMP has a key role in the regulation of the Hla and S. aureus-induced autophagic response. We present evidence that EPAC and Rap2b, through calpains activation, are the proteins involved in the regulation of Hla and S. aureus-induced autophagy. Interestingly, we showed that both, EPAC and Rap2b, are recruited to the S. aureus?containing phagosome. We believe that our findings have important implications in the understanding of the innate immune processes involved in intracellular pathogen invasion of the host cell.