aeruginosa and those isolated from chronic Silmitasertib order skin wounds with respect to the production of virulence determinants such as pyocyanin and extracellular protease. The six strains fell into three categories:
the first included the two type strains as well as one of the clinical isolates (PAO1, NCTC 6750 and 15159), the second contained the clinical isolates 23:1 and 27:1 and, finally, strain 14:2 (also a clinical isolate) formed a group on its own. In the first group, all strains expressed pyocyanin, elastase and alkaline proteinase, and two of the three produced the quorum-sensing molecule C4-HSL, while the second group showed no expression of C4-HSL or elastase. Interestingly, strain 14:2 was negative for the expression of C4-HSL, pyocyanin and the proteases. A similar spread in the expression of virulence factors and quorum-sensing molecules among P. aeruginosa strains has been described by others, for instance, Luzar & Montie (1985) and Lee et al. (2005), who investigated chronically
infected cystic fibrosis patients. Both studies showed not only variations between strains isolated from different patients but also changes associated with disease progression. Isolates from patients with more advanced disease showed lower pyocyanin and protease production, suggesting that the evolution of P. aeruginosa strains towards a less virulent phenotype may confer a survival advantage during chronic infection. Thus, in our study, the clinical isolate 14:2, which had selleck inhibitor the greatest inhibitory effect on biofilm formation by S. epidermidis and lacked the production of C4-HSL, pyocyanin and proteases, may represent a less virulent strain that has become adapted to enhance its persistence
in the chronic sore environment (Lee et al., 2005). In a recent study by Qin et al. (2009), extracellular products from P. aeruginosa were shown to disrupt S. epidermidis biofilms and it was suggested that extracellular polysaccharide could be responsible for the effect. Thus, the authors proposed that extracellular polysaccharides from P. aeruginosa may represent a novel target for the development of agents to control S. epidermidis biofilms at sites of infection. Mannose- and galactose-containing extracellular polysaccharides were detected in biofilms of all the strains of P. aeruginosa tested here, and thus the inhibition of S. epidermidis Calpain biofilm formation seen in our study may occur through a mechanism similar to that proposed by Qin and colleagues for biofilm dispersal. Expression of the two extracellular polysaccharides, Pel and Psl, is known to vary according to the strain and environmental conditions (Branda et al., 2005). Although 14:2 did not appear to produce higher levels of these polysaccharides than the other strains, which could account for its enhanced effect on S. epidermidis biofilms, it is possible that, for instance, differences in their relative expression may play an important role.