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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

Structure of natural and synthetic AHL-based compounds which inhibit biofilm formation by P. aeruginosa. (a) Native N-acyl-l-homoserine lactone, signal molecules of P. aeruginosa (C4-HSL and 3-oxo-C12-HSL), (b) synthetic analogue of AHLs with side aromatics and synthetic analogues of AHLs with modified lactone rings, and (c) natural (manoalide, penicillic acid, and patulin), and synthetic (furanones) compounds with lactone ring analogues.
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Related In: Results  -  Collection


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fig3: Structure of natural and synthetic AHL-based compounds which inhibit biofilm formation by P. aeruginosa. (a) Native N-acyl-l-homoserine lactone, signal molecules of P. aeruginosa (C4-HSL and 3-oxo-C12-HSL), (b) synthetic analogue of AHLs with side aromatics and synthetic analogues of AHLs with modified lactone rings, and (c) natural (manoalide, penicillic acid, and patulin), and synthetic (furanones) compounds with lactone ring analogues.

Mentions: QS is a cell-to-cell communication used by many bacteria to detect their population density by producing and perceiving diffusible signal molecules that coordinate virulence factors production, motility, and biofilm formation [53, 54]. P. aeruginosa possesses two main QS systems (las and rhl) which drive the production (throughout synthases LasI and RhlI) and the perception (by the transcription factors LasR and RhlR) of the autoinducer signaling molecules N-(3-oxododecanoyl)-L-homoserine lactone (3-oxo-C12-HSL) and N-butanoyl-L-homoserine lactone (C4-HSL) (Figure 3(a)), respectively [54]. A third QS system, based on quinolone signals (PQS system), interacts with the acyl homoserine lactones (AHLs) systems in an intricate way [54].


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)

Structure of natural and synthetic AHL-based compounds which inhibit biofilm formation by P. aeruginosa. (a) Native N-acyl-l-homoserine lactone, signal molecules of P. aeruginosa (C4-HSL and 3-oxo-C12-HSL), (b) synthetic analogue of AHLs with side aromatics and synthetic analogues of AHLs with modified lactone rings, and (c) natural (manoalide, penicillic acid, and patulin), and synthetic (furanones) compounds with lactone ring analogues.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig3: Structure of natural and synthetic AHL-based compounds which inhibit biofilm formation by P. aeruginosa. (a) Native N-acyl-l-homoserine lactone, signal molecules of P. aeruginosa (C4-HSL and 3-oxo-C12-HSL), (b) synthetic analogue of AHLs with side aromatics and synthetic analogues of AHLs with modified lactone rings, and (c) natural (manoalide, penicillic acid, and patulin), and synthetic (furanones) compounds with lactone ring analogues.
Mentions: QS is a cell-to-cell communication used by many bacteria to detect their population density by producing and perceiving diffusible signal molecules that coordinate virulence factors production, motility, and biofilm formation [53, 54]. P. aeruginosa possesses two main QS systems (las and rhl) which drive the production (throughout synthases LasI and RhlI) and the perception (by the transcription factors LasR and RhlR) of the autoinducer signaling molecules N-(3-oxododecanoyl)-L-homoserine lactone (3-oxo-C12-HSL) and N-butanoyl-L-homoserine lactone (C4-HSL) (Figure 3(a)), respectively [54]. A third QS system, based on quinolone signals (PQS system), interacts with the acyl homoserine lactones (AHLs) systems in an intricate way [54].

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