Serratia marcescens IS ABLE TO INVADE AND PERSIST INSIDE PHAGOCYTIC CELLS

JAVIER FERNANDO MARISCOTTI; ELEONORA GARCÍA VÉSCOVI

Mar del Plata

Congreso; X Congreso de Microbiología General SAMIGE 2014; 2014

Sociedad Argentina de Microbiología General (SAMIGE)

Serratia marcescens is an opportunistic human pathogen that represents a growing problem for public health, particularly in hospitalized or immunocompromised patients. Despite its clinical prevalence, factors and mechanisms that contribute to Serratia pathogenesis remain unclear. S. marcescens produces numerous exoproteins with toxic effects, including ShlA hemolysin that has been catalogued as a potent cytotoxin. In our previous work, we have shown that Serratia is able to invade, persist, and multiply inside non-phagocytic cells, residing in nonacidic, nondegradative, autophagosome-like vacuoles. In this host cells S. marcescens elicits an autophagic response. We determine that the ShlA is responsible for the autophagic response that is promoted previous to the bacteria internalization in host epithelial cells. We have recently observed that S. marcescens is able to escape from infected non-phagocytic cells in a ShlA-dependent manner. In this work, we have determined that the mutant strain shlB, which is unable to activate and secrete the ShlA hemolysin, increases up to 2-fold intracellular counts and decreases egress to the extracellular media. Other bacterial pathogens can infect a range of phagocytic and non-phagocytic cells during their life cycles. In this work, we analyse the invasion process of S. marcescens in phagocytic cells. We here show that S. marcescens is able to invade and persist inside of the murine macrophages cells RAW 264.7. We here analyse S. marcescens escape from infected phagocytic cells. Our results show that the bacterial intracellular increase of a shlB strain in infected phagocytic cells in the same manner that in non-phagocytic cells. This result suggests that the ShlA-dependent escape of S. marcescens from infected cells is a conserved mechanism that guarantees the spread of bacteria into the extracellular medium.