Staphylococcus aureus is a gram-positive pathogenic bacterium and is capable of secreting numerous toxins interfering directly with the host to cause acute infections. Rbf, a transcriptional regulator of AraC/XylS family, has been reported to promote biofilm formation in polysaccharide intercellular adhesion (PIA) mediated manner to cause chronic infections. In this study, we revealed the new virulence-mediated role of Rbf that can negatively regulate the hemolytic activity. Furthermore, Rbf can specifically bind to the hla and psmα promoters to repress their expression, resulting in significantly decreased production of phenol-soluble modulins α (PSMα) and alpha-toxin. Accordingly, the rbf mutant strain exhibited the increased pathogenicity compared to the wild-type (WT) strain in a mouse subcutaneous abscess model, representing a type of acute infection by S. aureus. Collectively, our results provide a novel insight into the virulence regulation and acute infections mediated by Rbf in S. aureus.

金黄色葡萄球菌是革兰氏阳性致病菌，能够分泌大量直接干扰宿主的毒素，引起急性感染。据报道，Rbf是AraC / XylS家族的转录调节因子，可通过多糖细胞间粘附（PIA）介导的方式促进生物膜形成，从而引起慢性感染。在这项研究中，我们揭示了Rbf的新的毒力介导作用，可以消极地调节溶血活性。此外，Rbf可以与hla和psmα启动子特异性结合，从而抑制其表达，从而导致酚溶性调节蛋白α（PSMα）和α-毒素的产生显着降低。因此，rbf在小鼠皮下脓肿模型中，该突变株与野生型（WT）株相比显示出更高的致病性，代表一种金黄色葡萄球菌的急性感染。总的来说，我们的结果为金黄色葡萄球菌中Rbf介导的毒力调节和急性感染提供了新颖的见解。