However, when grouped, CF isolates were found to form an amount of biofilm significantly lower compared to that observed among non-CF isolates. To exclude the possibility that these differences in biofilm formation could arise from differences in growth efficiency [36], biofilm levels were normalized on growth rate calculated for each strain. Although the mean growth Selleck PLX4032 rate of CF isolates was significantly lower than non-CF

ones – probably because of the phenotypic regulation of virulence factor expression by quorum sensing mechanisms or by in vivo bacterial microevolution driven by selective lung environmental conditions, mechanisms already described in bacteria [37–39] – significant differences in biofilm formation were maintained also after normalization, thus indicating that in S. maltophilia biofilm formation is not influenced by growth rate. The reduced efficiency in forming biofilm and the increased mean generation time exhibited by CF isolates could be the consequences of S. maltophilia adaptation to a stressed environment such as OSI-906 supplier CF lung [40–42]. To verify this hypothesis, five isogenic sequential S. maltophilia strains isolated from the same CF patient over a period of 3 years were investigated

for phenotypic variations. Our results showed that isogenic serial strains significantly differ in biofilm forming ability, susceptibility to oxidative stress, and swimming motility suggesting that different Etofibrate S. maltophilia phenotypes evolve within the CF respiratory tract during chronic infection. Particularly, the reduction in biofilm formation ability of sequential isolates is suggestive for the phenotypic conversion of S. maltophilia during chronic infection.

CLSM analysis showed that isolates from the early periods of chronic infection were able to form uniform flat biofilms or highly structured, multilayered and exopolysaccharide matrix-encased, biofilms. On the contrary, isolates recovered from the late phase of chronic infection showed a significant reduction in adherence, lacking ability to form a mature biofilm. Significant differences were also found with regard to susceptibility to oxidative stress and swimming motility. These results suggest that the onset of chronic infection could be transformative for S. maltophilia, probably reflecting an adaptive behavior that enables S. maltophilia to survive to the environmental stresses that are likely to be encountered within the habitat of the CF lung, such as (oxidative stress) low free iron, and anaerobic conditions [43]. In support of this, the phenotypic changes observed in P. aeruginosa isolates collected during different periods of chronic infection from CF patients, included loss of flagella or pilus mediated motility, loss of O antigen components of the LPS, as well as appearance of auxotrophic variants [39, 41, 44].