maltophilia GSK2118436 in vitro strains may persist in CF patients pulmonary tissue for up to 3 years, and that many patients are colonized at the same time with multiple strains of S. maltophilia [30]. Invasion of epithelial respiratory cells has been reported for CF-derived S. maltophilia clinical isolates [10, 20]. We have recently reported that, with the exception of an environmental S. maltophilia isolate (strain LMG959) all the CF-derived strains assayed were able to invade A549 cells

[20]. In the present study we evaluated the ability of twelve S. maltophilia CF isolates to invade IB3-1 cells, by classical invasion assays. The results obtained clearly indicated, for the first time, that S. maltophilia CF isolates were able to invade IB3-1 cells, albeit at a very low level (data not shown). Since strains presented a significant degree of heterogeneity in internalization efficiencies, it might be possible to hypothesize that S. maltophilia entry within IB3-1 cells AZ 628 ic50 may be strain-dependent. Together with the ability to form biofilm, the capability of S. maltophilia to enter IB3-1 might also explain the tendency of this microorganism to become persistent

within CF pulmonary tissues, since within intracellular compartments it could find protection against host defenses and the reach of antibiotics. Moreover, internalization may likely influence the modulation Crizotinib of the inflammatory response of the infected host. It has been reported that flagella could act as adhesins which play a role in bacterial binding to host mucosal surfaces as well as to abiotic surfaces [22, 31]. To study the role of flagella in the adhesiveness of S. maltophilia, we generated two independent mutants presenting a deletion encompassing the fliI gene of S. maltophilia strains OBGTC9 and OBGTC10. fliI encodes a substrate-specific ATPase (FliI), an enzyme necessary to provide energy for the export of flagellar structural components in a wide range of bacterial

species [32]. Swimming ability of the two mutant strains was almost completely abolished (Figure 4B). When co-cultured with IB3-1 cell monolayers, the two mutants showed a reduced capacity to adhere to IB3-1 cells, if compared to that of parental wild type strains (Figure 4A). Further, we showed that Bupivacaine neither swimming nor twitching motilities were significantly associated to adhesion to or biofilm formation on IB3-1 cells. Thus, taken together, our results suggest that although flagella must play some role in S. maltophilia adhesiveness, regardless of their functionality, other structures must also be involved in this phenomenon, since the fliI mutation only attenuates, but not abolishes, the ability of S. maltophilia strains to adhere to IB3-1 cells. We were not able to assess the role of flagella in S. maltophilia biofilm formation since exposure of IB3-1 monolayers to fliI – mutant strains caused their disruption already after 6h-exposure.