Regulation of Staphylococcus aureus induced Autophagy by protein kinase C.

GAURÓN, MARIA CELESTE; COLOMBO, M. I.

Mar del Plata, Argentina.

Congreso; LI Reunion SAIB; 2015

SAIB (Sociedad Argentina de Investigación en Bioquímica y Biología Molecular)

Autophagy is a degradative cellular process in response to stress or infection with certain pathogens. Some pathogens are able to modify the autophagic pathway in order to survive and replicate in the host cell. Staphylococcus aureus is a microorganism that causes serious diseases in humans. We have previously demonstrated that the virulence factor alfa-hemolysin (Hla) is responsible of the autophagic response induced by S. aureus. This factor is used by the microorganism for escaping from its containing phagosome labelled with the autophagic protein LC3. Interestingly, we have found that the autophagic response induced by this bacterium is independent of the canonical PI3K/Beclin1 pathway and it is, instead, regulated by an AMPc/EPAC/Rap2b pathway. It is known that certain species of Staphylococcus segregates PLC that generates DAG, which can recruit PKC from the host cells triggering an intracellular signalling pathway. In our current study we have found that certain PKCs isoforms regulate the autophagic response induced by S. aureus Noteworthy, both a classical and a novel PKC isoforms are able to inhibit the recruitment of LC3 to the bacterial phagosome, altering the intracellular replication of thepathogen. In addition, we have found that one of these isoforms is recruited to the S. aureus-containing phagosome in a Hla-dependent manner. Taken together our results strongly suggest that S. aureus modulates the association of PKCs to generate a more propitious replication niche before escaping to the cytoplasm.