Rsp promotes the transcription of virulence factors in an -independent manner in .

is a major human pathogen that causes a great diversity of community- and hospital-acquired infections. Rsp, a member of AraC/XylS family of transcriptional regulators (AFTRs), has been reported to play an important role in the regulation of virulence determinants in via an -dependent pathway. Here we demonstrated that Rsp could bind to the promoter to positively regulate its own expression. We then constructed an isogenic deletion strain and compared the haemolysis in the wild-type and mutant strains. Our results indicated that the mutant strain displayed decreased haemolytic activity, which was correlated with a dramatic decrease in the expression of and . Furthermore, we analysed the regulatory effects of Rsp in the mutant strain and found that they are -independent. Electrophoretic mobility shift assay indicated that Rsp can directly bind to the promoter regions of and . The mouse model of subcutaneous abscess showed that the mutant strain displayed a significant defect in virulence compared to the wild-type strain. These findings reveal that Rsp positively regulates the virulence of by promoting the expression of and through direct binding to their promoter regions.