Serratia marcescens invades epithelial cells and finds a suitable niche to survive and replicate.

FEDRIGO, G.V.; CAMPOY, E.; COLOMBO, M. I.; GARCIA VESCOVI, E.

Tucumán

Congreso; SAIB; 2009

Serratia marcescens INVADES EPITHELIAL CELLS AND FINDS A SUITABLE NICHE TO SURVIVE AND REPLICATE Fedrigo GV; Campoy EM; Colombo MI and García Véscovi E. IBR-CONICET, U.N.R., Rosario; IHEM-CONICET U.N. Cuyo, Mendoza. E-mail: fedrigo@ibr.gov.ar S. marcescens is an opportunistic human pathogen associated mainly with urinary and respiratory tract infections. This microorganism produces several extracellular proteins but there are evidences that only haemolysin ShlA and protease PrtA are able to act as virulence factors. However, the mechanisms that Serratia employs to disseminate in eukaryotic cells are presently unknown. In this work, we demonstrated that a clinical S. marcescens isolate was able to invade and multiply in CHO epithelial cells. Confocal microscopy analysis revealed that, since early stages after entry, intracellular bacteria colocalized with markers of early and late endosomes and this colocalization was maintained until six hours post-infection. In addition, S. marcescens colocalized with the autophagosomal marker LC3, being induction of autophagy blocked by inhibition of bacterial de novo protein synthesis. Moreover, Serratia was unable to replicate in atg5 knock-out mouse embryonic fibroblasts. ShlA expression from a non-pathogenic E. coli strain was able to induce cells autophagy from the extracellular space, suggesting that this factor is involved in the Serratia invasion process. Based on these findings, we propose that S. marcescens delays phagosome maturation and actively induces an authophagy-like process that might favour the intracellular survival and proliferation of the bacteria inside the host.