AUTHOR=Pompilio Arianna , Crocetta Valentina , De Nicola Serena , Verginelli Fabio , Fiscarelli Ersilia , Di Bonaventura Giovanni 

TITLE=Cooperative pathogenicity in cystic fibrosis: Stenotrophomonas maltophilia modulates Pseudomonas aeruginosa virulence in mixed biofilm

JOURNAL=Frontiers in Microbiology

VOLUME=6

YEAR=2015

URL=https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2015.00951

DOI=10.3389/fmicb.2015.00951

ISSN=1664-302X

ABSTRACT=<p>The present study was undertaken in order to understand more about the interaction occurring between <italic>S. maltophilia</italic> and <italic>P. aeruginosa</italic>, which are frequently co-isolated from CF airways. For this purpose, <italic>S. maltophilia</italic> RR7 and <italic>P. aeruginosa</italic> RR8 strains, co-isolated from the lung of a chronically infected CF patient during a pulmonary exacerbation episode, were evaluated for reciprocal effect during planktonic growth, adhesion and biofilm formation onto both polystyrene and CF bronchial cell monolayer, motility, as well as for gene expression in mixed biofilms. <italic>P. aeruginosa</italic> significantly affected <italic>S. maltophilia</italic> growth in both planktonic and biofilm cultures, due to an inhibitory activity probably requiring direct contact. Conversely, no effect was observed on <italic>P. aeruginosa</italic> by <italic>S. maltophilia</italic>. Compared with monocultures, the adhesiveness of <italic>P. aeruginosa</italic> on CFBE41o- cells was significantly reduced by <italic>S. maltophilia</italic>, which probably acts by reducing <italic>P. aeruginosa's</italic> swimming motility. An opposite trend was observed for biofilm formation, confirming the findings obtained using polystyrene. When grown in mixed biofilm with <italic>S. maltophilia, P. aeruginosa</italic> significantly over-expressed <italic>aprA</italic>, and <italic>algD</italic>—codifying for protease and alginate, respectively—while the quorum sensing related <italic>rhlR</italic> and <italic>lasI</italic> genes were down-regulated. The induced alginate expression by <italic>P. aeruginosa</italic> might be responsible for the protection of <italic>S. maltophilia</italic> against tobramycin activity we observed in mixed biofilms. Taken together, our results suggest that the existence of reciprocal interference of <italic>S. maltophilia</italic> and <italic>P. aeruginosa</italic> in CF lung is plausible. In particular, <italic>S. maltophilia</italic> might confer some selective “fitness advantage” to <italic>P. aeruginosa</italic> under the specific conditions of chronic infection or, alternatively, increase the virulence of <italic>P. aeruginosa</italic> thus leading to pulmonary exacerbation.</p>