Adherence of Staphylococcus aureus to endothelial cells: Influence of capsular polysaccharide, global regulator agr, and bacterial growth phase

The adherence of Staphylococcus aureus to human endothelial cells (EC) is p robably an important step in the pathogenesis of systemic staphylococcal in fections. We examined the influence of type 5 capsular polysaccharide (CP5) production, the global regulator agr, and the bacterial growth phase on S. aureus adherence to EC. Whereas S. aureus Newman showed maximal adherence to EC in the logarithmic phase of growth, an isogenic agr mutant showed max imal adherence in the stationary growth phase. S. aureus adherence to EC an d CP5 expression were negatively correlated: a mutation in the agr locus di minished CP5 production and led to increased adherence. Likewise, induction of CP5 expression by addition of NaCl to the growth medium resulted in red uced staphylococcal adherence to EC. S. aureus Newman cells that adhered to EC did not express CP5. A Newman cap50 mutant was acapsular and showed sig nificantly greater adherence to EC than the parental strain did (P < 0.005) . Complementation of the cap50 mutation in trans restored CP5 expression an d reduced EC adherence to a level similar to that of the parental strain. T he enhanced adherence shown by the cap50 mutant was similar in magnitude to that of the agr mutant or the cap50 agr double mutant. Cells of the cap50 mutant and cap50 agr double mutant harvested from stationary-phase cultures adhered significantly better than did cells harvested in the exponential g rowth phase. These data are consistent with the postexponential and agr-ind ependent expression by S. aureus of at least one putative EC adhesin, whose binding domain may be masked by CP5.