Phytochemical Compounds Targeting the Quorum Sensing System as a Tool to Reduce the Virulence Factors of Food Pathogenic Bacteria

Author(s):  
Jesus M. Luna-Solorza ◽  
Francisco J. Vazquez-Armenta ◽  
A. Thalia Bernal-Mercado ◽  
M. Melissa Gutierrez-Pacheco ◽  
Filomena Nazzaro ◽  
...  
MedChemComm ◽  
2015 ◽  
Vol 6 (2) ◽  
pp. 259-272 ◽  
Author(s):  
Ravindra Pal Singh

Quorum quenching compounds blocked quorum sensing system of bacteria by several mechanisms (a, b, c and d).


2008 ◽  
Vol 190 (21) ◽  
pp. 7043-7051 ◽  
Author(s):  
John M. Farrow ◽  
Zoe M. Sund ◽  
Matthew L. Ellison ◽  
Dana S. Wade ◽  
James P. Coleman ◽  
...  

ABSTRACT Pseudomonas aeruginosa is an opportunistic pathogen that causes both acute and chronic infections in immunocompromised individuals. This gram-negative bacterium produces a battery of virulence factors that allow it to infect and survive in many different hostile environments. The control of many of these virulence factors falls under the influence of one of three P. aeruginosa cell-to-cell signaling systems. The focus of this study, the quinolone signaling system, functions through the Pseudomonas quinolone signal (PQS), previously identified as 2-heptyl-3-hydroxy-4-quinolone. This signal binds to and activates the LysR-type transcriptional regulator PqsR (also known as MvfR), which in turn induces the expression of the pqsABCDE operon. The first four genes of this operon are required for PQS synthesis, but the fifth gene, pqsE, is not. The function of the pqsE gene is not known, but it is required for the production of multiple PQS-controlled virulence factors and for virulence in multiple models of infection. In this report, we show that PqsE can activate PQS-controlled genes in the absence of PqsR and PQS. Our data also suggest that the regulatory activity of PqsE requires RhlR and indicate that a pqsE mutant can be complemented for pyocyanin production by a large excess of exogenous N-butyryl homoserine lactone (C4-HSL). Finally, we show that PqsE enhances the ability of Escherichia coli expressing RhlR to respond to C4-HSL. Overall, our data lead us to conclude that PqsE functions as a regulator that is independent of PqsR and PQS but dependent on the rhl quorum-sensing system.


2013 ◽  
Vol 62 (3) ◽  
pp. 243-251 ◽  
Author(s):  
LIN LIHUA ◽  
WANG JIANHUI ◽  
YU JIALIN ◽  
LI YAYIN ◽  
LIU GUANXIN

The Gram-negative Pseudomonas aeruginosa bacterial pathogen is reputed for its resistance to multiple antibiotics, and this property is strongly associated with the development of biofilms. Bacterial biofilms form by aggregation of microorganisms on a solid surface and secretion of an extracellular polysaccharide substances that acts as a physical protection barrier for the encased bacteria. In addition, the P aeruginosa quorum-sensing system contributes to antibiotic resistance by regulating the expression of several virulence factors, including exotoxin A, elastase, pyoverdin and rhamnolipid. The organosulfur compound allicin, derived from garlic, has been shown to inhibit both surface-adherence of bacteria and production of virulence factors. In this study, the effects of allicin on P aeruginosa biofilm formation and the production of quorum-sensing controlled virulence factors were investigated. The results demonstrated that allicin could inhibit early bacterial adhesion, reduce EPS secretion, and down-regulate virulence factors' production. Collectively, these findings suggest the potential of allicin as a therapeutic agent for controlling P aeruginosa biofilm.


Author(s):  
Nicole Hugouvieux‐Cotte‐Pattat ◽  
Monique Royer ◽  
Erwan Gueguen ◽  
Paul Le Guen ◽  
Roderich D. Süssmuth ◽  
...  

1998 ◽  
Vol 66 (6) ◽  
pp. 2521-2528 ◽  
Author(s):  
Douglas G. Storey ◽  
Eva E. Ujack ◽  
Harvey R. Rabin ◽  
Ian Mitchell

ABSTRACT The role of Pseudomonas aeruginosa quorum-sensing systems in the lung infections associated with cystic fibrosis (CF) has not been examined. The purpose of this study was to determine if genes regulated by the LasR-LasI quorum-sensing system were coordinately regulated by the P. aeruginosa populations during the lung infections associated with CF. We also wanted to ascertain if there was a relationship between the expression of lasR, a transcriptional regulator, and some P. aeruginosa virulence factors during these infections. We extracted RNAs from the bacterial populations of 131 sputa taken from 23 CF patients. These RNAs were blotted and hybridized with probes to P. aeruginosa lasA,lasB, and toxA. The hybridization signals from each probe were ranked, and the rankings were analyzed by a Spearman rank correlation to determine if there was an association between the population transcript accumulations for the three genes. The correlations between the transcript accumulation patterns of pairs of the genes suggested that lasA, lasB, andtoxA might be coordinately regulated during CF lung infections. To determine if this coordinate regulation might be due to regulation by LasR, we probed RNAs, extracted from 84 sputa, with thelasR, lasA, lasB, toxA, and algD probes. Statistical analysis indicated thatlasR transcript accumulation correlated tolasA, lasB, toxA, andalgD transcript accumulations. These results indicated thatlasR may at least partially regulate or be coordinately regulated with lasA, lasB, toxA, and algD during the lung infections associated with CF. These results also suggested that the LasR-LasI quorum-sensing system may control the expression of at least some virulence factors in the lungs of patients with CF.


1998 ◽  
Vol 66 (9) ◽  
pp. 4499-4502 ◽  
Author(s):  
Christian Van Delden ◽  
Everett C. Pesci ◽  
James P. Pearson ◽  
Barbara H. Iglewski

ABSTRACT The las quorum-sensing system of Pseudomonas aeruginosa controls the expression of elastase and rhamnolipid. We report that starvation can select a mutant producing these virulence factors in spite of a lasR deletion. Expression of the autoinducer synthase gene rhlI was increased in this suppressor mutant, suggesting compensation by the rhlsystem. These data show that P. aeruginosa can restore elastase and rhamnolipid production in the absence of a functionallas quorum-sensing system.


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