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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

Kinetics of adhesion onto polystyrene by S. maltophilia RR7 and P. aeruginosa RR8, considered both as alone and in combination. Adhesion was assessed, after 3 h of incubation at 37°C, both by crystal violet and viable count assays. (A) Crystal violet assay. S. maltophilia RR7, and P. aeruginosa RR8 were tested both alone (RR7, RR8), and in mixed infection (RR7 + RR8), and the results are shown as mean + SD (n = 6). **p < 0.01, ***p < 0.001, ANOVA + Newman-Keuls post-test. (B) Viable count assay. S. maltophilia RR7 and P. aeruginosa RR8 strains were tested both alone (RR7, RR8), and in mixed infection (RR7combi, RR8combi), and the results are shown as mean + SD (n = 6). No statistically significant differences were found among groups by ANOVA + Newman-Keuls post-test. (C) Competitive index (CI; black bars) and Relative Increase Ratio (RIR; gray bars), calculated from single and dual cultures of S. maltophilia RR7 and P. aeruginosa RR8. The results are shown as mean ± SD (n = 6). CI vs. RIR, no statistically significant difference, unpaired t-test.
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Figure 2: Kinetics of adhesion onto polystyrene by S. maltophilia RR7 and P. aeruginosa RR8, considered both as alone and in combination. Adhesion was assessed, after 3 h of incubation at 37°C, both by crystal violet and viable count assays. (A) Crystal violet assay. S. maltophilia RR7, and P. aeruginosa RR8 were tested both alone (RR7, RR8), and in mixed infection (RR7 + RR8), and the results are shown as mean + SD (n = 6). **p < 0.01, ***p < 0.001, ANOVA + Newman-Keuls post-test. (B) Viable count assay. S. maltophilia RR7 and P. aeruginosa RR8 strains were tested both alone (RR7, RR8), and in mixed infection (RR7combi, RR8combi), and the results are shown as mean + SD (n = 6). No statistically significant differences were found among groups by ANOVA + Newman-Keuls post-test. (C) Competitive index (CI; black bars) and Relative Increase Ratio (RIR; gray bars), calculated from single and dual cultures of S. maltophilia RR7 and P. aeruginosa RR8. The results are shown as mean ± SD (n = 6). CI vs. RIR, no statistically significant difference, unpaired t-test.

Mentions: The interaction during adhesion phase between S. maltophilia RR7 and P. aeruginosa RR8 strains was assessed, tested as single and mixed cultures, after 3 h-incubation, both by crystal violet and the viable count assays; the results are reported in Figure 2.


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)

Kinetics of adhesion onto polystyrene by S. maltophilia RR7 and P. aeruginosa RR8, considered both as alone and in combination. Adhesion was assessed, after 3 h of incubation at 37°C, both by crystal violet and viable count assays. (A) Crystal violet assay. S. maltophilia RR7, and P. aeruginosa RR8 were tested both alone (RR7, RR8), and in mixed infection (RR7 + RR8), and the results are shown as mean + SD (n = 6). **p < 0.01, ***p < 0.001, ANOVA + Newman-Keuls post-test. (B) Viable count assay. S. maltophilia RR7 and P. aeruginosa RR8 strains were tested both alone (RR7, RR8), and in mixed infection (RR7combi, RR8combi), and the results are shown as mean + SD (n = 6). No statistically significant differences were found among groups by ANOVA + Newman-Keuls post-test. (C) Competitive index (CI; black bars) and Relative Increase Ratio (RIR; gray bars), calculated from single and dual cultures of S. maltophilia RR7 and P. aeruginosa RR8. The results are shown as mean ± SD (n = 6). CI vs. RIR, no statistically significant difference, unpaired t-test.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 2: Kinetics of adhesion onto polystyrene by S. maltophilia RR7 and P. aeruginosa RR8, considered both as alone and in combination. Adhesion was assessed, after 3 h of incubation at 37°C, both by crystal violet and viable count assays. (A) Crystal violet assay. S. maltophilia RR7, and P. aeruginosa RR8 were tested both alone (RR7, RR8), and in mixed infection (RR7 + RR8), and the results are shown as mean + SD (n = 6). **p < 0.01, ***p < 0.001, ANOVA + Newman-Keuls post-test. (B) Viable count assay. S. maltophilia RR7 and P. aeruginosa RR8 strains were tested both alone (RR7, RR8), and in mixed infection (RR7combi, RR8combi), and the results are shown as mean + SD (n = 6). No statistically significant differences were found among groups by ANOVA + Newman-Keuls post-test. (C) Competitive index (CI; black bars) and Relative Increase Ratio (RIR; gray bars), calculated from single and dual cultures of S. maltophilia RR7 and P. aeruginosa RR8. The results are shown as mean ± SD (n = 6). CI vs. RIR, no statistically significant difference, unpaired t-test.
Mentions: The interaction during adhesion phase between S. maltophilia RR7 and P. aeruginosa RR8 strains was assessed, tested as single and mixed cultures, after 3 h-incubation, both by crystal violet and the viable count assays; the results are reported in Figure 2.

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