S. marcescens EXPRESS THE FLAGELLUM INSIDE EPITHELIAL CELLS

JAVIER FERNANDO MARISCOTTI; ELEONORA GARCÍA VÉSCOVI

Buenos Aires

Congreso; REUNIÓN CONJUNTA DE SOCIEDADES DE BIOCIENCIAS; 2017

SOCIEDAD ARGENTINA DE INVESTIGACIÓN BIOQUÍMICA Y BIOLOGÍA MOLECULAR

Serratia marcescens (Sma) 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 Sma pathogenesis remain unclear. Sma ability to adapt to and survive in both hostile or changing environments also relates to the bacterial capacity to express a wide range of secreted enzymes, including lipases, phospholipases, hemolysin, proteases and nucleases. In our previous work, we have shown that Sma is able to invade, persist, and multiply inside non-phagocytic cells, residing in nonacidic, nondegradative, autophagosome-like vacuoles. In these host cells Sma elicits an autophagic response. We determined that the hemolysin ShlA is responsible for the autophagic response that is promoted previous to the bacteria internalization in host epithelial cells. Recently, our group demonstrated that Sma is able to escape from infected non-phagocytic cells in a ShlA-dependent manner. We demonstrated that flagellar expression was essential for the bacteria to adhere to epithelial cells and that this contact was required for subsequent internalization in nonphagocytic cells, suggesting that Sma flagellar apparatus components can act as adhesins. In this work, we analyse the expression of flagella in the invasion process of Sma in non-phagocytic cells. Results of indirect immunofluorescence assay using either confocal or fluorescence microscopy showed that Sma is able to express flagella inside of epithelial cells. We here also analyse the ability to re-infect epithelial cells of the bacteria that escape from infected cells. Our results show that the bacteria that egress from infected cells increase up to 2-fold the capacity to invade naïve epithelial cells than planktonic bacteria. The results suggest that flagellar expression within infected cells are involved in the capacity of Serratia to successfully spread to new cells.