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Background    Enterococcus faecalis  is one of the leading agents of nosocomial infections. To cause diseases, pathogens or opportunistic bacteria have to adapt and survive to the defense systems encountered in the host. One of the most important compounds of the host innate defense response against invading microorganisms is lysozyme. It is found in a wide variety of body fluids, as well as in cells of the innate immune system. Lysozyme could act either as a muramidase and/or as a cationic antimicrobial peptide. Like  Staphylococcus aureus ,  E. faecalis  is one of the few bacteria that are completely lysozyme resistant.    Results  This study revealed that  oatA  ( O -acetyl transferase) and  dlt  (D-Alanylation of lipoteicoic acids) genes contribute only partly to the lysozyme resistance of  E. faecalis  and that a specific transcriptional regulator, the extracytoplasmic function SigV sigma factor plays a key role in this event. Indeed, the  sigV  single mutant is as sensitive as the  oatA/dltA  double mutant, and the  sigV/oatA/dltA  triple mutant displays the highest level of lysozyme sensitivity suggesting synergistic effects of these genes. In  S. aureus , mutation of both  oatA  and  dlt  genes abolishes completely the lysozyme resistance, whereas this is not the case in  E. faecalis . Interestingly SigV does not control neither  oatA  nor  dlt  genes. Moreover, the  sigV  mutants clearly showed a reduced capacity to colonize host tissues, as they are significantly less recovered than the parental JH2-2 strain from organs of mice subjected to intravenous or urinary tract infections.    Conclusions  This work led to the discovery of an original model of lysozyme resistance mechanism which is obviously more complex than those described for other Gram positive pathogens. Moreover, our data provide evidences for a direct link between lysozyme resistance and virulence of  E. faecalis.

The Extracytoplasmic Function Sigma Factor SigV Plays a Key Role in the Original Model of Lysozyme Resistance and Virulence of Enterococcus faecalis