maltophilia strains, both from hospitalized CF and non-CF patients [21–32]. Our results confirmed the high degree of diversity between GDC-0973 cell line isolates from hospitalized CF and non-CF patients, click here thus suggesting that CF pulmonary S. maltophilia infections are mainly associated with a predominant strain. Nevertheless, we observed several examples of PFGE types shared by multiple isolates in both CF (pulsotypes 23.1 and 24.1) and non-CF (pulsotypes 1.1, 2.1, and 3.1) patients. In particular, the major PFGE type 23 clone identified, represented by 4 strains recovered from non replicate CF patients, likely indicate the occurrence

of person-to-person transmission of S. maltophilia strains, the acquisition of this specific clone

from a common source, or an independent acquisition of a widely-spread strain type. The dissemination and spread of a specific clone may be due to the circulation of a transmissible strain among CF patients, probably due to a better fitness of this specific clone in the CF pulmonary niche or from an environmental source. Interestingly, distinct PFGE types were found between CHIR-99021 in vitro CF isolates and non-CF isolates. Further studies are warranted to evaluate if factors associated to the virulence could affect this important segregation among these two settings. These results could reflect an extensive spread of S. maltophilia in the environment thus suggesting the existence of natural reservoirs of bacterial strains able to cause pathogenicity once acquired by CF patients. Contrary to P. aeruginosa, it has not been reported yet that S. maltophilia is capable of making the transition from an environmental state to a colonizing state in CF patients. However, Marzuillo et al [33] found a persistence of the

same S. maltophilia strain in water, taps, and sinks of different rooms of an Italian CF center, although no correlation was observed between clinical and water-associated isolates. Furthermore, we recently observed that environmental S. maltophilia is potentially virulent, although to HSP90 a lesser extent than CF one, in a murine model of lung infection [34]. Moreover, our results showed that two environmental isolates (C34, A33) shared genetically related PFGE type with a non-CF isolate (Sm184). Thus, it is plausible to hypothesize that the acquisition of pathogenic S. maltophilia strains can occur directly from the natural environment. S. maltophilia is capable of adhering to and forming biofilm not only on polystyrene [12–14, 16, 35], but also on CF bronchial epithelial cells [17], suggesting that biofilm formation could be a critical step in colonisation of CF lung. While S. maltophilia possesses complex, diversified genomes [1] and forms biofilms, it is not yet known whether there are any variations in biofilm formation among clonally diverse clinical and environmental isolates.