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The formation of biofilms by Pseudomonas aeruginosa: a review of the natural and synthetic compounds interfering with control mechanisms.

Rasamiravaka T, Labtani Q, Duez P, El Jaziri M - Biomed Res Int (2015)

Bottom Line: Beyond its natural resistance to many drugs, its ability to form biofilm, a complex biological system, renders ineffective the clearance by immune defense systems and antibiotherapy.The objective of this report is to provide an overview (i) on P. aeruginosa biofilm lifestyle cycle, (ii) on the main key actors relevant in the regulation of biofilm formation by P. aeruginosa including QS systems, GacS/GacA and RetS/LadS two-component systems and C-di-GMP-dependent polysaccharides biosynthesis, and (iii) finally on reported natural and synthetic products that interfere with control mechanisms of biofilm formation by P. aeruginosa without affecting directly bacterial viability.Concluding remarks focus on perspectives to consider biofilm lifestyle as a target for eradication of resistant infections caused by P. aeruginosa.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Plant Biotechnology, Université Libre de Bruxelles, rue des Professeurs Jeener et Brachet 12, 6041 Gosselies, Belgium.

ABSTRACT
P. aeruginosa is an opportunistic pathogenic bacterium responsible for both acute and chronic infections. Beyond its natural resistance to many drugs, its ability to form biofilm, a complex biological system, renders ineffective the clearance by immune defense systems and antibiotherapy. The objective of this report is to provide an overview (i) on P. aeruginosa biofilm lifestyle cycle, (ii) on the main key actors relevant in the regulation of biofilm formation by P. aeruginosa including QS systems, GacS/GacA and RetS/LadS two-component systems and C-di-GMP-dependent polysaccharides biosynthesis, and (iii) finally on reported natural and synthetic products that interfere with control mechanisms of biofilm formation by P. aeruginosa without affecting directly bacterial viability. Concluding remarks focus on perspectives to consider biofilm lifestyle as a target for eradication of resistant infections caused by P. aeruginosa.

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Related in: MedlinePlus

P. aeruginosa biofilm phenotypes and effectiveness of tobramycin treatment in presence of DMSO 1% or coumarate ester (CE) at 300 µg/mL. (a) After 1 day of incubation, P. aeruginosa fails to form structured confluent aggregate in presence of CE as compared to DMSO treatment. (b) CE considerably increases the susceptibility of P. aeruginosa to tobramycin (100 µg/mL), as shown by the increased proportion of dead cells compared with DMSO. The bacterial viability was assessed by staining the cells with SYTO-9 (green areas—live bacteria) and propidium iodide (red areas—dead bacteria) furnished in the LIVE/DEAD BacLight kit. Cells were visualized using a Leica DM IRE2 inverted fluorescence microscope using a 40x objective lens and colored images were assembled using Adobe Photoshop.
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fig5: P. aeruginosa biofilm phenotypes and effectiveness of tobramycin treatment in presence of DMSO 1% or coumarate ester (CE) at 300 µg/mL. (a) After 1 day of incubation, P. aeruginosa fails to form structured confluent aggregate in presence of CE as compared to DMSO treatment. (b) CE considerably increases the susceptibility of P. aeruginosa to tobramycin (100 µg/mL), as shown by the increased proportion of dead cells compared with DMSO. The bacterial viability was assessed by staining the cells with SYTO-9 (green areas—live bacteria) and propidium iodide (red areas—dead bacteria) furnished in the LIVE/DEAD BacLight kit. Cells were visualized using a Leica DM IRE2 inverted fluorescence microscope using a 40x objective lens and colored images were assembled using Adobe Photoshop.

Mentions: The flavan-3-ol catechin, isolated from the bark of Combretum albiflorum (Tul.) Jongkind, as well as the flavanone naringenin, both at 4 mM final concentration, do interfere with QS mechanism in P. aeruginosa PAO1 by affecting autoinducers perception and biofilm formation [124–126]. A coumarate ester isolated from the bark extract of Malagasy endemic Dalbergia trichocarpa Baker interferes with P. aeruginosa QS systems (las and rhl), inhibits the biofilm formation and increases the effectiveness of the antibiotic tobramycin in killing biofilm-encapsulated P. aeruginosa [126] (Figures 4 and 5).


The formation of biofilms by Pseudomonas aeruginosa: a review of the natural and synthetic compounds interfering with control mechanisms.

Rasamiravaka T, Labtani Q, Duez P, El Jaziri M - Biomed Res Int (2015)

P. aeruginosa biofilm phenotypes and effectiveness of tobramycin treatment in presence of DMSO 1% or coumarate ester (CE) at 300 µg/mL. (a) After 1 day of incubation, P. aeruginosa fails to form structured confluent aggregate in presence of CE as compared to DMSO treatment. (b) CE considerably increases the susceptibility of P. aeruginosa to tobramycin (100 µg/mL), as shown by the increased proportion of dead cells compared with DMSO. The bacterial viability was assessed by staining the cells with SYTO-9 (green areas—live bacteria) and propidium iodide (red areas—dead bacteria) furnished in the LIVE/DEAD BacLight kit. Cells were visualized using a Leica DM IRE2 inverted fluorescence microscope using a 40x objective lens and colored images were assembled using Adobe Photoshop.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4383298&req=5

fig5: P. aeruginosa biofilm phenotypes and effectiveness of tobramycin treatment in presence of DMSO 1% or coumarate ester (CE) at 300 µg/mL. (a) After 1 day of incubation, P. aeruginosa fails to form structured confluent aggregate in presence of CE as compared to DMSO treatment. (b) CE considerably increases the susceptibility of P. aeruginosa to tobramycin (100 µg/mL), as shown by the increased proportion of dead cells compared with DMSO. The bacterial viability was assessed by staining the cells with SYTO-9 (green areas—live bacteria) and propidium iodide (red areas—dead bacteria) furnished in the LIVE/DEAD BacLight kit. Cells were visualized using a Leica DM IRE2 inverted fluorescence microscope using a 40x objective lens and colored images were assembled using Adobe Photoshop.
Mentions: The flavan-3-ol catechin, isolated from the bark of Combretum albiflorum (Tul.) Jongkind, as well as the flavanone naringenin, both at 4 mM final concentration, do interfere with QS mechanism in P. aeruginosa PAO1 by affecting autoinducers perception and biofilm formation [124–126]. A coumarate ester isolated from the bark extract of Malagasy endemic Dalbergia trichocarpa Baker interferes with P. aeruginosa QS systems (las and rhl), inhibits the biofilm formation and increases the effectiveness of the antibiotic tobramycin in killing biofilm-encapsulated P. aeruginosa [126] (Figures 4 and 5).

Bottom Line: Beyond its natural resistance to many drugs, its ability to form biofilm, a complex biological system, renders ineffective the clearance by immune defense systems and antibiotherapy.The objective of this report is to provide an overview (i) on P. aeruginosa biofilm lifestyle cycle, (ii) on the main key actors relevant in the regulation of biofilm formation by P. aeruginosa including QS systems, GacS/GacA and RetS/LadS two-component systems and C-di-GMP-dependent polysaccharides biosynthesis, and (iii) finally on reported natural and synthetic products that interfere with control mechanisms of biofilm formation by P. aeruginosa without affecting directly bacterial viability.Concluding remarks focus on perspectives to consider biofilm lifestyle as a target for eradication of resistant infections caused by P. aeruginosa.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Plant Biotechnology, Université Libre de Bruxelles, rue des Professeurs Jeener et Brachet 12, 6041 Gosselies, Belgium.

ABSTRACT
P. aeruginosa is an opportunistic pathogenic bacterium responsible for both acute and chronic infections. Beyond its natural resistance to many drugs, its ability to form biofilm, a complex biological system, renders ineffective the clearance by immune defense systems and antibiotherapy. The objective of this report is to provide an overview (i) on P. aeruginosa biofilm lifestyle cycle, (ii) on the main key actors relevant in the regulation of biofilm formation by P. aeruginosa including QS systems, GacS/GacA and RetS/LadS two-component systems and C-di-GMP-dependent polysaccharides biosynthesis, and (iii) finally on reported natural and synthetic products that interfere with control mechanisms of biofilm formation by P. aeruginosa without affecting directly bacterial viability. Concluding remarks focus on perspectives to consider biofilm lifestyle as a target for eradication of resistant infections caused by P. aeruginosa.

Show MeSH
Related in: MedlinePlus