Regulation of Staphylococcus aureus induced Autophagy by protein kinase C. LI Reunion SAIB. 3 al 6 de noviembre 2015. Mar del Plata, Argentina.

GAURÓN, MC; COLOMBO M.I.

Mar del Plata

Congreso; LI Reunion SAIB. 3 al 6 de noviembre 2015.; 2015

SAIB

Autophagy is a degradative cellular process in response to stress or infection with certain pathogens. Some pathogensare able to modify this pathway in order to survive and replicate in the host cell. We have previously demonstratedthat the virulence factor alfa-hemolysin (Hla) is responsible of the autophagic response induced by Staphylococcusaureus. This toxin is used by the pathogen for escaping from its containing phagosome labelled with the autophagicprotein LC3. We have found that the autophagic response induced by this bacterium is independent of thePI3K/Beclin1 pathway and it is, instead, regulated by an AMPc/EPAC/Rap2b pathway. It´s known that species ofStaphylococcus segregates PLC that generates DAG, which can recruit PKC from the host cells triggering aBIOCELL 39 (Suppl. 2) 2015signalling pathway. In our current study we have found that certain PKCs isoforms regulate the autophagic responseinduced by S. aureus. Noteworthy, both a classical and a novel PKC isoforms are able to inhibit the recruitment ofLC3 to the bacterial phagosome, altering the intracellular replication of the pathogen. In addition, we have found thatone of these isoforms is recruited to the S. aureus-containing phagosome in a Hla-dependent manner. Taken togetherour results strongly suggest that S. aureus modulates the association of PKCs to generate a more propitiousreplication niche before escaping to the cytoplasm