Staphylococcus epidermidis ΔSortase A strain elicits protective immunity against Staphylococcus aureus infection

Staphylococcus aureus and Staphylococcus epidermidis are two of the most significant opportunistic human pathogens, causing medical implant and nosocomial infections worldwide. These bacteria contain surface proteins that play crucial roles in multiple biological processes. It has become apparent that they have evolved a number of unique mechanisms by which they can immobilise proteins on their surface. Notably, a conserved cell membrane-anchored enzyme, sortase A (SrtA), can catalyse the covalent attachment of precursor bacterial cell wall-attached proteins to peptidoglycan. Considering its indispensable role in anchoring substrates to the cell wall and its effects on virulence, SrtA has attracted great attention. In this study, a 549-bp gene was cloned from a pathogenic S. epidermidis strain, YC-1, which shared high identity with srtA from other Staphylococcus spp. A mutant strain, YC-1ΔsrtA, was then constructed by allelic exchange mutagenesis. The direct survival rate assay suggested that YC-1ΔsrtA had a lower survival capacity in healthy mice blood compare with the wild-type strain, indicating that the deletion of srtA affects the virulence and infectious capacity of S. epidermidis YC-1. YC-1ΔsrtA was then administered via intraperitoneal injection and it provided a relative percent survival value of 72.7 % in mice against S. aureus TC-1 challenge. These findings demonstrate the possbility that YC-1ΔsrtA might be used as a live attenuated vaccine to produce cross-protection against S. aureus.