SAM performed bioinformatics analyses, participated in its design and coordination and helped to draft the manuscript. CWP performed transmission electron microscopy. JH designed and produced the microarrays, conceived the transcriptome experimental design, and helped analyze the array data. POT conceived the study, and participated in its design and coordination and drafted the manuscript.

All authors read and approved learn more the final manuscript.”
“Background Cystic fibrosis (CF) is a common inherited genetic disorder, caused by a mutation in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) protein [1] which is expressed in many different cells. In the lung, the derived chloride transport defect leads to altered airway physiology including impairment of mucociliary clearance, production of plugs of thick mucus and impaired innate immunity [2, 3]. These defects predispose the CF patient to microbial colonization and thus, to infections that tend to become chronic. The likelihood of contracting chronic infections increases with age and Pseudomonas aeruginosa becomes the dominant infecting microorganism, KU55933 with a colonization percentage varying from 42 to 100% [4]. Recently, Stenotrophomonas maltophilia has gained considerable attention as an important emerging nosocomial pathogen able to cause infections in debilitated and immunocompromised patients, as well as in CF patients [5, 6]. Colonization of the pulmonary tissues occurs in

approximately one third of CF patients, nevertheless, there is controversy as whether S. maltophilia colonization leads to a poorer clinical outcome or morbidity [7–9]. Persistent colonization by P. aeruginosa and the attendant damage of the epithelial mucosa by released pseudomonal exoproducts may increase the probability that S. maltophilia will colonize the respiratory tract of CF patients and significantly contribute to the progressive deterioration of their pulmonary functions [10, 11]. However, the mechanism of pathogenicity enabling S. maltophilia to establish infection and chronic colonization of the respiratory tract of CF patients remains

largely unexplored. Bumetanide Biofilm formation is increasingly recognized as an important bacterial virulence trait contributing to disease progression in CF and other diseases of the respiratory tract associated with chronic infections. Biofilm growth is believed to protect bacteria from natural immune defenses, as well as from the actions of several antibiotic compounds [12, 13]. P. aeruginosa strains isolated from the sputum of CF patients display morphologic and physiologic characteristics suggestive of in vivo biofilm formation, including over a 1000-fold increase in antibiotic resistance and a significant ability in evading host defense factors [14–17]. S. maltophilia has been recently reported to be able to adhere to cultured epithelial respiratory cells, as well as to produce biofilm on a variety of abiotic surfaces [10, 18, 19].