Amphypterygium adstringens Anacardic Acid Mixture Inhibits Quorum Sensing-controlled Virulence Factors of Chromobacterium violaceum and Pseudomonas aeruginosa

2013 ◽  
Vol 44 (7) ◽  
pp. 488-494 ◽  
Author(s):  
Israel Castillo-Juárez ◽  
Rodolfo García-Contreras ◽  
Norma Velázquez-Guadarrama ◽  
Marcos Soto-Hernández ◽  
Mariano Martínez-Vázquez
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Virulence Factors ◽  
Chromobacterium Violaceum ◽  
Anacardic Acid ◽  
Acid Mixture

scholarly journals A Quorum-Sensing Inhibitor Strain of Vibrio alginolyticus Blocks Qs-Controlled Phenotypes in Chromobacterium violaceum and Pseudomonas aeruginosa

Marine Drugs ◽  
2019 ◽  
Vol 17 (9) ◽  
pp. 494 ◽  
Author(s):  
José Carlos Reina ◽  
Ignacio Pérez-Victoria ◽  
Jesús Martín ◽  
Inmaculada Llamas
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Virulence Factors ◽  
Bacterial Infections ◽  
Fermentation Broth ◽  
Vibrio Alginolyticus ◽  
Chromobacterium Violaceum ◽  
Rrna Gene ◽  
Sea Anemones ◽  
Quorum Sensing Inhibitor

The cell density-dependent mechanism, quorum sensing (QS), regulates the expression of virulence factors. Its inhibition has been proposed as a promising new strategy to prevent bacterial pathogenicity. In this study, 827 strains from the microbiota of sea anemones and holothurians were screened for their ability to produce quorum-sensing inhibitor (QSI) compounds. The strain M3-10, identified as Vibrio alginolyticus by 16S rRNA gene sequencing, as well as ANIb and dDDH analyses, was selected for its high QSI activity. Bioassay-guided fractionation of the cell pellet extract from a fermentation broth of strain M3-10, followed by LC–MS and NMR analyses, revealed tyramine and N-acetyltyramine as the active compounds. The QS inhibitory activity of these molecules, which was confirmed using pure commercially available standards, was found to significantly inhibit Chromobacterium violaceum ATCC 12472 violacein production and virulence factors, such as pyoverdine production, as well as swarming and twitching motilities, produced by Pseudomonas aeruginosa PAO1. This constitutes the first study to screen QSI-producing strains in the microbiota of anemones and holothurians and provides an insight into the use of naturally produced QSI as a possible strategy to combat bacterial infections.

scholarly journals Evaluation of Anti-quorum Sensing Potential of Saraca asoca (Family Caesalpiniaceae) against Chromobacterium violaceum and Pseudomonas aeruginosa PA01

2021 ◽  
pp. 71-82
Author(s):  
B. S. Paliya ◽  
J. Mathew ◽  
B. N. Singh
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Virulence Factors ◽  
Test Sample ◽  
Stem Bark ◽  
Chromobacterium Violaceum ◽  
Broth Culture ◽  
Bark Extract ◽  
Swarming Motility ◽  
Saraca Asoca

Aim: The present study was performed to evaluate the anti-quorum sensing (QS) potential of traditional medicinal herb Saracaasoca (family Caesalpiniaceae) stem bark extract against Chromobacterium violaceum and Pseudomonas aeruginosa PA01. Study Design: First, the test sample (bark extract) was screened for anti-QS activity. Then systematic in-vitro and biochemical tests were performed to evaluate the effect of the test sample on the QS mediated virulence factors. Place and Duration of Study: All the experimental works were performed in Lab 311, pharmacology division, CSIR-NBRI Lucknow from June 2019 to October 2019. Methodology: The samples of Saraca asoca stem bark were washed, dried and extracted using 70% methanol. The minimum inhibitory concentration (MIC) of the prepared Sarca asoca bark extract was determined using the Alamar blue assay, and the anti-QS activity was screened using standard agar overlay method against CV 12472 at subinhibitory concentrations 100, 200 and 300 µg (< MIC value). SAE effect on biofilms formation was assessed by growing biofilms on glass slides in a static culture of PA01. Anti-virulence effect of SAE on the production of QS-regulated virulence factors such as Pyocyanin, proteases, elastases, rhamnolipid and alginate in Pseudomonas aeruginosa was determined using the supernatant of a 24 hours old broth culture of PA01 supplemented with SAE. Using the agar plate technique, the swimming and swarming motility assays were conducted on 0.3% and 0.5% agar plates respectively. One-way ANOVA was used to analyze the data, presented as mean ± SD (standard deviation) of three independent experiments. Results: Preliminary screening results showed significant QS inhibition against CV 12472 in an agar overlay disk diffusion assay in a concentration-dependent manner. Data from the biofilm assay showed loose, distorted, irregular PA01 biofilm formation at 200 µg (48%) and 300 µg (65%). SAE caused a significant drop in virulence factor production, with maximum reduction in pyocyanin (58%), proteases (67%), elastases (52%), rhamnolipid (53%), and alginate (44%) observed at 300 µg concentration. At SAE sub-lethal concentrations (200 and 300 µg), both the swimming and swarming motility of PA01 were significantly inhibited. Conclusions: The present study demonstrates the broad-spectrum anti-QS potential of SAE, reported for the first time, suggesting that SAE could be considered as an alternative herbal source to develop antimicrobial agents which can be either solitary or synergistically with conventional antimicrobial drugs.

scholarly journals Pseudomonas aeruginosa PA80 is a cystic fibrosis isolate deficient in RhlRI quorum sensing

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Syed A. K. Shifat Ahmed ◽  
Michelle Rudden ◽  
Sabrina M. Elias ◽  
Thomas J. Smyth ◽  
Roger Marchant ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Virulence Factors ◽  
Genomic Islands ◽  
Clinical Strain ◽  
Whole Genome ◽  
Synonymous Mutations ◽  
Wide Range

AbstractPseudomonas aeruginosa uses quorum sensing (QS) to modulate the expression of several virulence factors that enable it to establish severe infections. The QS system in P. aeruginosa is complex, intricate and is dominated by two main N-acyl-homoserine lactone circuits, LasRI and RhlRI. These two QS systems work in a hierarchical fashion with LasRI at the top, directly regulating RhlRI. Together these QS circuits regulate several virulence associated genes, metabolites, and enzymes in P. aeruginosa. Paradoxically, LasR mutants are frequently isolated from chronic P. aeruginosa infections, typically among cystic fibrosis (CF) patients. This suggests P. aeruginosa can undergo significant evolutionary pathoadaptation to persist in long term chronic infections. In contrast, mutations in the RhlRI system are less common. Here, we have isolated a clinical strain of P. aeruginosa from a CF patient that has deleted the transcriptional regulator RhlR entirely. Whole genome sequencing shows the rhlR locus is deleted in PA80 alongside a few non-synonymous mutations in virulence factors including protease lasA and rhamnolipid rhlA, rhlB, rhlC. Importantly we did not observe any mutations in the LasRI QS system. PA80 does not appear to have an accumulation of mutations typically associated with several hallmark pathoadaptive genes (i.e., mexT, mucA, algR, rpoN, exsS, ampR). Whole genome comparisons show that P. aeruginosa strain PA80 is closely related to the hypervirulent Liverpool epidemic strain (LES) LESB58. PA80 also contains several genomic islands (GI’s) encoding virulence and/or resistance determinants homologous to LESB58. To further understand the effect of these mutations in PA80 QS regulatory and virulence associated genes, we compared transcriptional expression of genes and phenotypic effects with isogenic mutants in the genetic reference strain PAO1. In PAO1, we show that deletion of rhlR has a much more significant impact on the expression of a wide range of virulence associated factors rather than deletion of lasR. In PA80, no QS regulatory genes were expressed, which we attribute to the inactivation of the RhlRI QS system by deletion of rhlR and mutation of rhlI. This study demonstrates that inactivation of the LasRI system does not impact RhlRI regulated virulence factors. PA80 has bypassed the common pathoadaptive mutations observed in LasR by targeting the RhlRI system. This suggests that RhlRI is a significant target for the long-term persistence of P. aeruginosa in chronic CF patients. This raises important questions in targeting QS systems for therapeutic interventions.

scholarly journals Revisiting the quorum-sensing hierarchy in Pseudomonas aeruginosa: the transcriptional regulator RhlR regulates LasR-specific factors

Microbiology ◽  
2009 ◽  
Vol 155 (3) ◽  
pp. 712-723 ◽  
Author(s):  
Valérie Dekimpe ◽  
Eric Déziel
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Virulence Factors ◽  
Transcriptional Regulator ◽  
Homoserine Lactone ◽  
The Other ◽  
Virulence Determinants ◽  
Late Stationary Phase ◽  
Regulatory Systems ◽  
Specific Factors

Pseudomonas aeruginosa uses the two major quorum-sensing (QS) regulatory systems las and rhl to modulate the expression of many of its virulence factors. The las system is considered to stand at the top of the QS hierarchy. However, some virulence factors such as pyocyanin have been reported to still be produced in lasR mutants under certain conditions. Interestingly, such mutants arise spontaneously under various conditions, including in the airways of cystic fibrosis patients. Using transcriptional lacZ reporters, LC/MS quantification and phenotypic assays, we have investigated the regulation of QS-controlled factors by the las system. Our results show that activity of the rhl system is only delayed in a lasR mutant, thus allowing the expression of multiple virulence determinants such as pyocyanin, rhamnolipids and C4-homoserine lactone (HSL) during the late stationary phase. Moreover, at this stage, RhlR is able to overcome the absence of the las system by activating specific LasR-controlled functions, including production of 3-oxo-C12-HSL and Pseudomonas quinolone signal (PQS). P. aeruginosa is thus able to circumvent the deficiency of one of its QS systems by allowing the other to take over. This work demonstrates that the QS hierarchy is more complex than the model simply presenting the las system above the rhl system.

scholarly journals The YebC Family Protein PA0964 Negatively Regulates the Pseudomonas aeruginosa Quinolone Signal System and Pyocyanin Production

2008 ◽  
Vol 190 (18) ◽  
pp. 6217-6227 ◽  
Author(s):  
Haihua Liang ◽  
Lingling Li ◽  
Zhaolin Dong ◽  
Michael G. Surette ◽  
Kangmin Duan
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Virulence Factors ◽  
Response Regulator ◽  
Initial Study ◽  
Pfam Family ◽  
Swarming Motility ◽  
Sensing Systems ◽  
Family Protein ◽  
Pyocyanin Production

ABSTRACT Bacterial pathogenicity is often manifested by the expression of various cell-associated and secreted virulence factors, such as exoenzymes, protease, and toxins. In Pseudomonas aeruginosa, the expression of virulence genes is coordinately controlled by the global regulatory quorum-sensing systems, which includes the las and rhl systems as well as the Pseudomonas quinolone signal (PQS) system. Phenazine compounds are among the virulence factors under the control of both the rhl and PQS systems. In this study, regulation of the phzA1B1C1D1E1 (phzA1) operon, which is involved in phenazine synthesis, was investigated. In an initial study of inducing conditions, we observed that phzA1 was induced by subinhibitory concentrations of tetracycline. Screening of 13,000 mutants revealed 32 genes that altered phzA1 expression in the presence of subinhibitory tetracycline concentrations. Among them, the gene PA0964, designated pmpR ( p qsR-mediated P QS r egulator), has been identified as a novel regulator of the PQS system. It belongs to a large group of widespread conserved hypothetical proteins with unknown function, the YebC protein family (Pfam family DUF28). It negatively regulates the quorum-sensing response regulator pqsR of the PQS system by binding at its promoter region. Alongside phzA1 expression and phenazine and pyocyanin production, a set of virulence factors genes controlled by both rhl and the PQS were shown to be modulated by PmpR. Swarming motility and biofilm formation were also significantly affected. The results added another layer of regulation in the rather complex quorum-sensing systems in P. aeruginosa and demonstrated a clear functional clue for the YebC family proteins.

Possible antivirulent activity of some agents against clinical isolates of Pseudomonas aeruginosa

2021 ◽  
Vol 30 (2) ◽  
pp. 1-8
Author(s):  
Ahmad O. Rifai ◽  
Abeer M. Abd El-Aziz ◽  
Hany I. Kenawy
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Virulence Factors ◽  
Therapeutic Target ◽  
Inhibitory Action ◽  
Antibacterial Agents ◽  
Mechanisms Of Resistance ◽  
Life Threatening ◽  
Pheniramine Maleate ◽  
Pyocyanin Production

Background: Pseudomonas aeruginosa has developed different mechanisms of resistance against antibiotics and became one of the most life-threatening pathogens. Fighting against its virulence Factors are an alternative therapeutic target. Objective: This study was directed towards the investigation of anti-quorum sensing activity and inhibitory action on virulence factors of different agents including antibacterial agents to which Pseudomonas aeruginosa isolates are resistant and non-antibacterial agents. Methodology: Anti-quorum sensing activity of ceftriaxone, ceftazidime (CAZ), cefepime (FEP), vancomycin (VA), paracetamol (PA), and pheniramine maleate (PHE) investigated as well as their ability to reduce other virulence factors including protease, hemolysin, and pyocyanin production. Results: This study showed that 3rd and 4th generations cephalosporins could be used as anti-quorum sensing agents effectively in the treatment of Pseudomonas aeruginosa infections, however, vancomycin, paracetamol, and pheniramine maleate had no effect on inhibiting the studied virulence factors. Conclusion: From our study we conclude that although cephalosporins at the used concentrations did not show anti-pseudomonal activity they were effective as anti virulent agents that could be utilized in therapeutically in controlling Pseudomonas aeruginosa infections.

scholarly journals Interference with Pseudomonas aeruginosa Quorum Sensing and Virulence by the Mycobacterial Pseudomonas Quinolone Signal Dioxygenase AqdC in Combination with the N-Acylhomoserine Lactone Lactonase QsdA

2019 ◽  
Vol 87 (10) ◽  
Author(s):  
Franziska S. Birmes ◽  
Ruth Säring ◽  
Miriam C. Hauke ◽  
Niklas H. Ritzmann ◽  
Steffen L. Drees ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Virulence Factors ◽  
Rhodococcus Erythropolis ◽  
Quorum Quenching ◽  
Signal Molecules ◽  
Content Type ◽  
Acylhomoserine Lactone ◽  
Regulatory Effects ◽  
Epithelial Lung Cells

ABSTRACT The nosocomial pathogen Pseudomonas aeruginosa regulates its virulence via a complex quorum sensing network, which, besides N-acylhomoserine lactones, includes the alkylquinolone signal molecules 2-heptyl-3-hydroxy-4(1H)-quinolone (Pseudomonas quinolone signal [PQS]) and 2-heptyl-4(1H)-quinolone (HHQ). Mycobacteroides abscessus subsp. abscessus, an emerging pathogen, is capable of degrading the PQS and also HHQ. Here, we show that although M. abscessus subsp. abscessus reduced PQS levels in coculture with P. aeruginosa PAO1, this did not suffice for quenching the production of the virulence factors pyocyanin, pyoverdine, and rhamnolipids. However, the levels of these virulence factors were reduced in cocultures of P. aeruginosa PAO1 with recombinant M. abscessus subsp. massiliense overexpressing the PQS dioxygenase gene aqdC of M. abscessus subsp. abscessus, corroborating the potential of AqdC as a quorum quenching enzyme. When added extracellularly to P. aeruginosa cultures, AqdC quenched alkylquinolone and pyocyanin production but induced an increase in elastase levels. When supplementing P. aeruginosa cultures with QsdA, an enzyme from Rhodococcus erythropolis which inactivates N-acylhomoserine lactone signals, rhamnolipid and elastase levels were quenched, but HHQ and pyocyanin synthesis was promoted. Thus, single quorum quenching enzymes, targeting individual circuits within a complex quorum sensing network, may also elicit undesirable regulatory effects. Supernatants of P. aeruginosa cultures grown in the presence of AqdC, QsdA, or both enzymes were less cytotoxic to human epithelial lung cells than supernatants of untreated cultures. Furthermore, the combination of both aqdC and qsdA in P. aeruginosa resulted in a decline of Caenorhabditis elegans mortality under P. aeruginosa exposure.

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