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The limited number of studies addressing the quorum response and staphylococcal 
biofilms appear at first glance to be somewhat conflicting in their results and 
interpretation. Pratten et al. 34 found little difference between wildtype S. 
aureus and an agr mutant in adherence to either uncoated or fibronectincoated 
glass under flow conditions even though hld was expressed. In another study 
RNAIII expression decreased S. aureus adherence to fibrinogen under static 
conditions but increased adherence to fibronectin and human endothelial cells 
in both static and flow conditions 35. Vuong et al. 36 found that those S. 
aureus strains with a nonfunctional agr were much more likely to form biofilms 
under static conditions. toxin positively regulated by the agr systemwas 
recently shown to be required for biofilm formation under both static and flow 
conditions 37. In an experimental endocarditis study RNAIII expression 
increased with increasing S. aureus densities in vegetations 38 confirming the 
cell densitydependent expression of RNAIII in vivo. Interestingly expression of 
RNAIII also occurred through a mechanism independent of the AgrAC signaling 
system suggesting that there are additional unidentified in vivo signals that 
regulate the quorum response. Taken together these studies indicate that the 
precise role of agr expression in biofilm development is dependent upon the 
conditions in which the biofilm is grown and suggest that differences in S. 
aureus strains may also introduce variability into the results. 






 
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