Adhesion to and biofilm formation on IB3-1 bronchial cells by Stenotrophomonas maltophilia isolates from cystic fibrosis patients

<p>Abstract</p> <p>Background</p> <p><it>Stenotrophomonas maltophilia </it>has recently gained considerable attention as an important emerging pathogen in cystic fibrosis (CF) patients. However, the role of this microorganism in the pathophysiology of CF lung disease remains largely unexplored. In the present study for the first time we assessed the ability of <it>S. maltophilia </it>CF isolates to adhere to and form biofilm in experimental infection experiments using the CF-derived bronchial epithelial IB3-1cell line. The role of flagella on the adhesiveness of <it>S. maltophilia </it>to IB3-1 cell monolayers was also assessed by using <it>fliI </it>mutant derivative strains.</p> <p>Results</p> <p>All <it>S. maltophilia </it>CF isolates tested in the present study were able, although at different levels, to adhere to and form biofilm on IB3-1 cell monolayers. Scanning electron and confocal microscopy revealed <it>S. maltophilia </it>structures typical of biofilm formation on bronchial IB3-1 cells. The loss of flagella significantly (P < 0.001) decreased bacterial adhesiveness, if compared to that of their parental flagellated strains. <it>S. maltophilia </it>CF isolates were also able to invade IB3-1 cells, albeit at a very low level (internalization rate ranged from 0.01 to 4.94%). Pre-exposure of IB3-1 cells to <it>P. aeruginosa </it>PAO1 significantly increased <it>S. maltophilia </it>adhesiveness. Further, the presence of <it>S. maltophilia </it>negatively influenced <it>P. aeruginosa </it>PAO1 adhesiveness.</p> <p>Conclusions</p> <p>The main contribution of the present study is the finding that <it>S. maltophilia </it>is able to form biofilm on and invade CF-derived IB3-1 bronchial epithelial cells, thus posing a rationale for the persistence and the systemic spread of this opportunistic pathogen in CF patients. Experiments using <it>in vivo </it>models which more closely mimic CF pulmonary tissues will certainly be needed to validate the relevance of our results.</p

Telomeres, telomerase and cardiac regeneration

The fundamental role of telomerase is to protect telomere length and maintain the potency of cell proliferation. Although increased telomerase activity is present in cardiac development or postinjury regeneration, repression of telomerase activity and expression seems to be independent of differentiation or cellular senescence. Telomerase maintains the proliferative capacity of myogenic stem cells by interacting with early transcription factors that drive cardiac development. Therefore, in addition to maintaining telomere length, telomerase also may be involved in regulation of cardiac specific gene expression, apoptosis, proliferation and differentiation. This can be explained by possible interactions of telomerase with cellular or nuclear proteins. In this chapter, we review recent studies of noncanonical roles of telomerase in cardiovascular development and repair.. Madonna, Rosalinda &amp; Renna, F.V. &amp; Confalone, Pat. (2015). Telomeres, telomerase and cardiac regeneration. The fundamental role of telomerase is to protect telomere length and maintain the potency of cell proliferation. Although increased telomerase activity is present in cardiac development or postinjury regeneration, repression of telomerase activity and expression seems to be independent of differentiation or cellular senescence. Telomerase maintains the proliferative capacity of myogenic stem cells by interacting with early transcription factors that drive cardiac development. Therefore, in addition to maintaining telomere length, telomerase also may be involved in regulation of cardiac specific gene expression, apoptosis, proliferation and differentiation. This can be explained by possible interactions of telomerase with cellular or nuclear proteins. In this chapter, we review recent studies of noncanonical roles of telomerase in cardiovascular development and repair