Regulation of Staphylococcus aureus immunodominant antigen B (IsaB)

Abstract

Staphylococcus aureus is a leading cause of nosocomial and community-acquired infections and increased prevalence of antibiotic resistance has necessitated the search for novel therapeutic targets. The immunodominant antigen B induces an antibody response during septicemia and has therefore been proposed as a vaccine target. Because it appears to be expressed during infection but not during colonization, we sought to characterize the regulation of isaB expression by internal transcription factors and external stimuli. We found that expression of isaB was stimulated by glucose, human serum, and plasma. Furthermore isaB transcript levels increased in the absence of the global staphylococcal accessory regulator SarA and decreased in the absence of the carbon catabolite regulator CcpA. Interestingly, glucose and CcpA-mediated isaB expression appeared to be related to the decrease in pH subsequent to carbon metabolism, rather than a direct response to the carbon source and could be prevented by buffering the growth medium.