Modulation of virulence gene expression in Staphylococcus aureus by interleukin-1beta: novel implications in bacterial pathogenesis.

The effect of IL-1beta on Staphylococcus aureus was investigated in terms of mRNA expression profile of bicomponent leukotoxins (Luk ED, Luk PV, HlgA, and HlgCB) as well as microbial surface components recognizing adhesive matrix molecules (MSCRAMMs). Upon exposure to higher concentrations of IL-1beta, S. aureus expressed significantly higher levels of MSCRAMMs mRNA [fibronectin-binding protein (FnBp), fibrinogen-binding protein or clumping factor (Clf), and collagen-binding protein (Cna)] and had significantly lower expression of mRNAs for bicomponent leukotoxins. Sequential in vitro passing of S. aureus in the absence of rhIL-1beta resulted in reduced binding to rhIL-1beta resulted in lack of significant changes in virulence gene expression upon exposure to low or high concentrations of rhIL-1beta. It is possible that IL-1beta modulates the pathogenic potential of S. aureus by altering its virulence gene expression to adapt to the host's inflammatory micromilieu. The ability to express higher levels of MSCRAMMs and low levels of leukotoxins might contribute towards the successful invasion and persistence of S. aureus in chronic inflammatory conditions. Determination of the mechanisms of IL-1-induced alterations in S. aureus gene expression may lead to the identification of novel therapeutic targets against this ever-evolving opportunistic pathogen.