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Mycofabricated biosilver nanoparticles interrupt Pseudomonas aeruginosa quorum sensing systems.

Singh BR, Singh BN, Singh A, Khan W, Naqvi AH, Singh HB - Sci Rep (2015)

Bottom Line: Transcriptional studies demonstrated that mfAgNPs reduced the levels of LasIR-RhlIR.Further genes quantification analyses revealed that mfAgNPs significantly down-regulated QS-regulated genes, specifically those encoded to the secretion of virulence factors.The results clearly indicated the anti-virulence property of mfAgNPs by inhibiting P. aeruginosa QS signaling.

View Article: PubMed Central - PubMed

Affiliation: Centre of Excellence in Materials Science (Nanomaterials), Z.H. College of Engineering &Technology, Aligarh Muslim University, Aligarh-202002, India.

ABSTRACT
Quorum sensing (QS) is a chemical communication process that Pseudomonas aeruginosa uses to regulate virulence and biofilm formation. Disabling of QS is an emerging approach for combating its pathogenicity. Silver nanoparticles (AgNPs) have been widely applied as antimicrobial agents against human pathogenic bacteria and fungi, but not for the attenuation of bacterial QS. Here we mycofabricated AgNPs (mfAgNPs) using metabolites of soil fungus Rhizopus arrhizus BRS-07 and tested their effect on QS-regulated virulence and biofilm formation of P. aeruginosa. Transcriptional studies demonstrated that mfAgNPs reduced the levels of LasIR-RhlIR. Treatment of mfAgNPs inhibited biofilm formation, production of several virulence factors (e.g. LasA protease, LasB elastrase, pyocyanin, pyoverdin, pyochelin, rhamnolipid, and alginate) and reduced AHLs production. Further genes quantification analyses revealed that mfAgNPs significantly down-regulated QS-regulated genes, specifically those encoded to the secretion of virulence factors. The results clearly indicated the anti-virulence property of mfAgNPs by inhibiting P. aeruginosa QS signaling.

No MeSH data available.


Related in: MedlinePlus

Possible anti-QS mechanism of mfAgNPs.P. aeruginosa uses Las-Rhl systems to produce signaling molecules (i.e. AHLs) intracellularly which then exported to the extracellular space to assess their cell density. Once a pre-determined level is exceeded, LuxR-AHLs complex activates the expression of target genes and this mechanism is called as QS. After cellular internalization of mfAgNPs might likely interact with PAO1QS systems, thereby inhibiting the LasIR-RhlIR-mediated AHLs production. In the absence of AHLs, LuxI and LuxR receptors do not bind to DNA, thereby inhibiting the expression of targeted genes which encode virulence factors and biofilms.
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f7: Possible anti-QS mechanism of mfAgNPs.P. aeruginosa uses Las-Rhl systems to produce signaling molecules (i.e. AHLs) intracellularly which then exported to the extracellular space to assess their cell density. Once a pre-determined level is exceeded, LuxR-AHLs complex activates the expression of target genes and this mechanism is called as QS. After cellular internalization of mfAgNPs might likely interact with PAO1QS systems, thereby inhibiting the LasIR-RhlIR-mediated AHLs production. In the absence of AHLs, LuxI and LuxR receptors do not bind to DNA, thereby inhibiting the expression of targeted genes which encode virulence factors and biofilms.

Mentions: The present study clearly demonstrated that mfAgNPs attenuated P. aeruginosa QS systems and biofilm formation without a significant effect on its growth (Fig. 7; Supplementary figures 6A, B and D). Production of violacein pigment by C. violaceum 12472 is regulated by AHL-mediated QS system. Inhibition of violacein production by mfAgNPs clearly confirmed their anti-QS activity in a concentration dependent manner. This is in accordance with the previous studies on the inhibition of violacein production by anti-QS nanomaterials3536. In addition, mfAgNPs inhibited the production of extracellular virulence factors including proteases, siderophores, rhamnolipid and alginate of PAO1. Moreover, higher stability of mfAgNPs was noticed at room temperature upto 330 days of incubation as well as in culture media for 72 h as compared to SBH-synthesized AgNPs (Supplementary figures 11A–E).


Mycofabricated biosilver nanoparticles interrupt Pseudomonas aeruginosa quorum sensing systems.

Singh BR, Singh BN, Singh A, Khan W, Naqvi AH, Singh HB - Sci Rep (2015)

Possible anti-QS mechanism of mfAgNPs.P. aeruginosa uses Las-Rhl systems to produce signaling molecules (i.e. AHLs) intracellularly which then exported to the extracellular space to assess their cell density. Once a pre-determined level is exceeded, LuxR-AHLs complex activates the expression of target genes and this mechanism is called as QS. After cellular internalization of mfAgNPs might likely interact with PAO1QS systems, thereby inhibiting the LasIR-RhlIR-mediated AHLs production. In the absence of AHLs, LuxI and LuxR receptors do not bind to DNA, thereby inhibiting the expression of targeted genes which encode virulence factors and biofilms.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4562228&req=5

f7: Possible anti-QS mechanism of mfAgNPs.P. aeruginosa uses Las-Rhl systems to produce signaling molecules (i.e. AHLs) intracellularly which then exported to the extracellular space to assess their cell density. Once a pre-determined level is exceeded, LuxR-AHLs complex activates the expression of target genes and this mechanism is called as QS. After cellular internalization of mfAgNPs might likely interact with PAO1QS systems, thereby inhibiting the LasIR-RhlIR-mediated AHLs production. In the absence of AHLs, LuxI and LuxR receptors do not bind to DNA, thereby inhibiting the expression of targeted genes which encode virulence factors and biofilms.
Mentions: The present study clearly demonstrated that mfAgNPs attenuated P. aeruginosa QS systems and biofilm formation without a significant effect on its growth (Fig. 7; Supplementary figures 6A, B and D). Production of violacein pigment by C. violaceum 12472 is regulated by AHL-mediated QS system. Inhibition of violacein production by mfAgNPs clearly confirmed their anti-QS activity in a concentration dependent manner. This is in accordance with the previous studies on the inhibition of violacein production by anti-QS nanomaterials3536. In addition, mfAgNPs inhibited the production of extracellular virulence factors including proteases, siderophores, rhamnolipid and alginate of PAO1. Moreover, higher stability of mfAgNPs was noticed at room temperature upto 330 days of incubation as well as in culture media for 72 h as compared to SBH-synthesized AgNPs (Supplementary figures 11A–E).

Bottom Line: Transcriptional studies demonstrated that mfAgNPs reduced the levels of LasIR-RhlIR.Further genes quantification analyses revealed that mfAgNPs significantly down-regulated QS-regulated genes, specifically those encoded to the secretion of virulence factors.The results clearly indicated the anti-virulence property of mfAgNPs by inhibiting P. aeruginosa QS signaling.

View Article: PubMed Central - PubMed

Affiliation: Centre of Excellence in Materials Science (Nanomaterials), Z.H. College of Engineering &Technology, Aligarh Muslim University, Aligarh-202002, India.

ABSTRACT
Quorum sensing (QS) is a chemical communication process that Pseudomonas aeruginosa uses to regulate virulence and biofilm formation. Disabling of QS is an emerging approach for combating its pathogenicity. Silver nanoparticles (AgNPs) have been widely applied as antimicrobial agents against human pathogenic bacteria and fungi, but not for the attenuation of bacterial QS. Here we mycofabricated AgNPs (mfAgNPs) using metabolites of soil fungus Rhizopus arrhizus BRS-07 and tested their effect on QS-regulated virulence and biofilm formation of P. aeruginosa. Transcriptional studies demonstrated that mfAgNPs reduced the levels of LasIR-RhlIR. Treatment of mfAgNPs inhibited biofilm formation, production of several virulence factors (e.g. LasA protease, LasB elastrase, pyocyanin, pyoverdin, pyochelin, rhamnolipid, and alginate) and reduced AHLs production. Further genes quantification analyses revealed that mfAgNPs significantly down-regulated QS-regulated genes, specifically those encoded to the secretion of virulence factors. The results clearly indicated the anti-virulence property of mfAgNPs by inhibiting P. aeruginosa QS signaling.

No MeSH data available.


Related in: MedlinePlus