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

Pompilio A, Crocetta V, De Nicola S, Verginelli F, Fiscarelli E, Di Bonaventura G - Front Microbiol (2015)

Bottom Line: Conversely, no effect was observed on P. aeruginosa by S. maltophilia.Compared with monocultures, the adhesiveness of P. aeruginosa on CFBE41o- cells was significantly reduced by S. maltophilia, which probably acts by reducing P. aeruginosa's swimming motility.Taken together, our results suggest that the existence of reciprocal interference of S. maltophilia and P. aeruginosa in CF lung is plausible.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical, Oral and Biotechnological Sciences, "G. d'Annunzio" University of Chieti-Pescara Chieti, Italy ; Aging Research Center (Ce.S.I.), "G. d'Annunzio" University Foundation Chieti, Italy.

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

No MeSH data available.


Related in: MedlinePlus

Adhesion and biofilm formation by S. maltophilia RR7 and P. aeruginosa RR8 onto CFBE41o- CF bronchial cells. CFBE41o- cell monolayers were exposed for (A) 3 h (adhesion assay) or (B) 24 h (biofilm formation assay) to S. maltophilia RR7 and P. aeruginosa RR8 (each at 106 CFU/ml; MOI: 10), tested as alone (RR7, RR8) or in mixed cultures (RR7combi, RR8combi). *p < 0.05, **p < 0.01, ANOVA + Newman-Keuls post-test. (C) In mixed cultures, the Competitive Index (CI) and the Relative Increase Ratio (RIR) were calculated as described in Materials and Methods. The results are shown as mean + SD (n = 6). **p < 0.01; unpaired t-test.
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Figure 4: Adhesion and biofilm formation by S. maltophilia RR7 and P. aeruginosa RR8 onto CFBE41o- CF bronchial cells. CFBE41o- cell monolayers were exposed for (A) 3 h (adhesion assay) or (B) 24 h (biofilm formation assay) to S. maltophilia RR7 and P. aeruginosa RR8 (each at 106 CFU/ml; MOI: 10), tested as alone (RR7, RR8) or in mixed cultures (RR7combi, RR8combi). *p < 0.05, **p < 0.01, ANOVA + Newman-Keuls post-test. (C) In mixed cultures, the Competitive Index (CI) and the Relative Increase Ratio (RIR) were calculated as described in Materials and Methods. The results are shown as mean + SD (n = 6). **p < 0.01; unpaired t-test.

Mentions: P. aeruginosa RR8 and S. maltophilia RR7 were evaluated, both alone and in mixed culture, for adhesion to, and biofilm formation onto, CFBE41o- CF cell monolayer. The results of the viable count assay are summarized in Figure 4.


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

Pompilio A, Crocetta V, De Nicola S, Verginelli F, Fiscarelli E, Di Bonaventura G - Front Microbiol (2015)

Adhesion and biofilm formation by S. maltophilia RR7 and P. aeruginosa RR8 onto CFBE41o- CF bronchial cells. CFBE41o- cell monolayers were exposed for (A) 3 h (adhesion assay) or (B) 24 h (biofilm formation assay) to S. maltophilia RR7 and P. aeruginosa RR8 (each at 106 CFU/ml; MOI: 10), tested as alone (RR7, RR8) or in mixed cultures (RR7combi, RR8combi). *p < 0.05, **p < 0.01, ANOVA + Newman-Keuls post-test. (C) In mixed cultures, the Competitive Index (CI) and the Relative Increase Ratio (RIR) were calculated as described in Materials and Methods. The results are shown as mean + SD (n = 6). **p < 0.01; unpaired t-test.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4584994&req=5

Figure 4: Adhesion and biofilm formation by S. maltophilia RR7 and P. aeruginosa RR8 onto CFBE41o- CF bronchial cells. CFBE41o- cell monolayers were exposed for (A) 3 h (adhesion assay) or (B) 24 h (biofilm formation assay) to S. maltophilia RR7 and P. aeruginosa RR8 (each at 106 CFU/ml; MOI: 10), tested as alone (RR7, RR8) or in mixed cultures (RR7combi, RR8combi). *p < 0.05, **p < 0.01, ANOVA + Newman-Keuls post-test. (C) In mixed cultures, the Competitive Index (CI) and the Relative Increase Ratio (RIR) were calculated as described in Materials and Methods. The results are shown as mean + SD (n = 6). **p < 0.01; unpaired t-test.
Mentions: P. aeruginosa RR8 and S. maltophilia RR7 were evaluated, both alone and in mixed culture, for adhesion to, and biofilm formation onto, CFBE41o- CF cell monolayer. The results of the viable count assay are summarized in Figure 4.

Bottom Line: Conversely, no effect was observed on P. aeruginosa by S. maltophilia.Compared with monocultures, the adhesiveness of P. aeruginosa on CFBE41o- cells was significantly reduced by S. maltophilia, which probably acts by reducing P. aeruginosa's swimming motility.Taken together, our results suggest that the existence of reciprocal interference of S. maltophilia and P. aeruginosa in CF lung is plausible.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical, Oral and Biotechnological Sciences, "G. d'Annunzio" University of Chieti-Pescara Chieti, Italy ; Aging Research Center (Ce.S.I.), "G. d'Annunzio" University Foundation Chieti, Italy.

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

No MeSH data available.


Related in: MedlinePlus