It is then tempting to speculate that the presence of HQNO will p

It is then tempting to speculate that the presence of HQNO will prevent S. aureus from disseminating and will rather favor tissue colonization, biofilm production and invasion of host cells. It has indeed been suggested that S. aureus FnBPs HKI-272 price mediates cellular

invasion [53, 54] whereas the capacity of the bacterium to remain intracellular is helped by the Sorafenib manufacturer repression of hla [55]. Accordingly, we showed that an exposure of S. aureus to HQNO up-regulates the expression of fnbA and represses the expression of hla. However, whether or not HQNO and P. aeruginosa increase the invasion of host cells by S. aureus remains to be confirmed. Interestingly, O’Neil et al. [32] have recently demonstrated that the FnBPs are also involved in the ica-independent Selleckchem Peptide 17 mechanism of biofilm formation. It is thus

possible that FnBPs are directly responsible for the observed HQNO-mediated SigB-dependent increase in biofilm production and, more specifically, FnBPA which is under the control of SigB for expression [15, 19, 22, 37]. As such, the FnBPs would represent the main effectors for both biofilm formation and cellular invasion in S. aureus SCVs. HQNO may be one of several bacterial exoproducts influencing S. aureus during polymicrobial Olopatadine infections. Our results and those of Machan et al. [47] suggest that other HAQs may also affect S. aureus, although not as efficiently as HQNO. Moreover, it is known that other P. aeruginosa exoproducts such as pyocyanin have an inhibitory activity against the electron transport chain of S. aureus [13]. Loss of pyocyanin production has been associated with mutations in the pqsA-E genes [45, 56], which may provide an additional explanation for the different effects of the pqsA and pqsL mutants we have observed on the growth (data not shown) and biofilm formation of S. aureus (Fig. 6C). Furthermore, Qazi et al. [7] found that an N-acyl-homoserine-lactone

from P. aeruginosa antagonizes quorum sensing and virulence gene expression in S. aureus. More precisely, it was shown that the 3-oxo-C12-HSL interacts with the cytoplasmic membrane of S. aureus and down-regulates both sarA and agr expression. Although we also observed here a down-regulation of agr, the HQNO-mediated up-regulation of sarA suggests further complexity in the response of S. aureus to P. aeruginosa exoproducts. It is possible that the outcome of the S. aureus-P. aeruginosa interaction is dependent on the amount and the types of exoproducts secreted by the specific strain of P. aeruginosa interacting with S. aureus.

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