Inhibition of the pqsABCDE and pqsH in the pqs quorum sensing system and related virulence factors of the Pseudomonas aeruginosa PAO1 strain by farnesol

2020 ◽  
Vol 151 ◽  
pp. 104956 ◽  
Author(s):  
Wen-Ru Li ◽  
Tao-Hua Zeng ◽  
Xiao-Bao Xie ◽  
Qing-Shan Shi ◽  
Cai-Ling Li
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Virulence Factors ◽  
Pseudomonas Aeruginosa Pao1 ◽  
Sensing System ◽  
Quorum Sensing System ◽  
Pao1 Strain

scholarly journals Effects of Allicin on the Formation of Pseudomonas aeruginosa Biofilm and the Production of Quorum-Sensing Controlled Virulence Factors

2013 ◽  
Vol 62 (3) ◽  
pp. 243-251 ◽  
Author(s):  
LIN LIHUA ◽  
WANG JIANHUI ◽  
YU JIALIN ◽  
LI YAYIN ◽  
LIU GUANXIN
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Virulence Factors ◽  
Bacterial Pathogen ◽  
Organosulfur Compound ◽  
Extracellular Polysaccharide ◽  
Sensing System ◽  
Quorum Sensing System ◽  
Extracellular Polysaccharide Substances ◽  
Multiple Antibiotics

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.

scholarly journals Quorum Sensing Regulates Denitrification in Pseudomonas aeruginosa PAO1

2007 ◽  
Vol 189 (13) ◽  
pp. 4969-4972 ◽  
Author(s):  
Masanori Toyofuku ◽  
Nobuhiko Nomura ◽  
Tatsuya Fujii ◽  
Naoki Takaya ◽  
Hideaki Maseda ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Homoserine Lactone ◽  
Anaerobic Growth ◽  
Signal Molecules ◽  
Pseudomonas Aeruginosa Pao1 ◽  
Sensing System ◽  
Quorum Sensing System ◽  
Denitrification Activity

ABSTRACT Anaerobic growth of Pseudomonas aeruginosa PAO1 was affected by quorum sensing. Deletion of genes that produce N-acyl-l-homoserine lactone signals resulted in an increase in denitrification activity, which was repressed by exogenous signal molecules. The effect of the las quorum-sensing system was dependent on the rhl quorum-sensing system in regulating denitrification.

scholarly journals Pseudomonas aeruginosa lasRTranscription Correlates with the Transcription of lasA,lasB, and toxA in Chronic Lung Infections Associated with Cystic Fibrosis

1998 ◽  
Vol 66 (6) ◽  
pp. 2521-2528 ◽  
Author(s):  
Douglas G. Storey ◽  
Eva E. Ujack ◽  
Harvey R. Rabin ◽  
Ian Mitchell
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Virulence Factors ◽  
Rank Correlation ◽  
Transcript Accumulation ◽  
Bacterial Populations ◽  
Sensing System ◽  
Quorum Sensing System ◽  
Lung Infections

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.

scholarly journals Starvation Selection Restores Elastase and Rhamnolipid Production in a Pseudomonas aeruginosaQuorum-Sensing Mutant

1998 ◽  
Vol 66 (9) ◽  
pp. 4499-4502 ◽  
Author(s):  
Christian Van Delden ◽  
Everett C. Pesci ◽  
James P. Pearson ◽  
Barbara H. Iglewski
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Virulence Factors ◽  
Rhamnolipid Production ◽  
Sensing System ◽  
Quorum Sensing System

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.

scholarly journals Regulation of Pseudomonas Quinolone Signal Synthesis in Pseudomonas aeruginosa

2005 ◽  
Vol 187 (13) ◽  
pp. 4372-4380 ◽  
Author(s):  
Dana S. Wade ◽  
M. Worth Calfee ◽  
Edson R. Rocha ◽  
Elizabeth A. Ling ◽  
Elana Engstrom ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Virulence Factors ◽  
Transcriptional Start Site ◽  
Opportunistic Pathogen ◽  
Homoserine Lactone ◽  
Mobility Shift ◽  
Sensing System ◽  
Regulator Protein ◽  
Quorum Sensing System

ABSTRACT Pseudomonas aeruginosa is an opportunistic pathogen that causes chronic lung infections in cystic fibrosis patients and is a major source of nosocomial infections. This bacterium controls many virulence factors by using two quorum-sensing systems, las and rhl. The las system is composed of the LasR regulator protein and its cell-to-cell signal, N-(3-oxododecanoyl) homoserine lactone, and the rhl system is composed of RhlR and the signal N-butyryl homoserine lactone. A third intercellular signal, the Pseudomonas quinolone signal (PQS; 2-heptyl-3-hydroxy-4-quinolone), also regulates numerous virulence factors. PQS synthesis requires the expression of multiple operons, one of which is pqsABCDE. Previous experiments showed that the transcription of this operon, and therefore PQS production, is negatively regulated by the rhl quorum-sensing system and positively regulated by the las quorum-sensing system and PqsR (also known as MvfR), a LysR-type transcriptional regulator protein. With the use of DNA mobility shift assays and β-galactosidase reporter fusions, we have studied the regulation of pqsR and its relationship to pqsA, lasR, and rhlR. We show that PqsR binds the promoter of pqsA and that this binding increases dramatically in the presence of PQS, implying that PQS acts as a coinducer for PqsR. We have also mapped the transcriptional start site for pqsR and found that the transcription of pqsR is positively regulated by lasR and negatively regulated by rhlR. These results suggest that a regulatory chain occurs where pqsR is under the control of LasR and RhlR and where PqsR in turn controls pqsABCDE, which is required for the production of PQS.

scholarly journals Pseudomonas aeruginosa Regulatory Protein AnvM Controls Pathogenicity in Anaerobic Environments and Impacts Host Defense

mBio ◽  
2019 ◽  
Vol 10 (4) ◽  
Author(s):  
Yingchao Zhang ◽  
Chuan-min Zhou ◽  
Qinqin Pu ◽  
Qun Wu ◽  
Shirui Tan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Immune Response ◽  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Anaerobic Conditions ◽  
Content Type ◽  
Sensing System ◽  
Quorum Sensing System ◽  
Aerobic And Anaerobic ◽  
Aerobic And Anaerobic Conditions

ABSTRACT Pseudomonas aeruginosa, one of the most common pathogens in hospital-acquired infections, is tightly controlled by a multilayered regulatory network, including the quorum sensing system (QS), the type VI secretion system (T6SS), and resistance to host immunity. We found that the P. aeruginosa 3880 (PA3880) gene, which encodes an unknown protein, acts as a regulator of anaerobic metabolism in response to oxidative stress and virulence in P. aeruginosa. More than 30 PA3880 homologs were found in other bacterial genomes, indicating that PA3880 is widely distributed in the Bacteria kingdom as a highly conserved gene. Deletion of the PA3880 gene changed the expression levels of more than 700 genes, including a group of virulence genes, under both aerobic and anaerobic conditions. To further study the mechanisms of PA3880-mediated regulation in virulence, we utilized a bacterial two-hybrid assay and found that the PA3880 protein interacted directly with QS regulator MvfR and anaerobic regulator Anr. Loss of the PA3880 protein significantly blunted the pathogenicity of P. aeruginosa, resulting in increased host survival, decreased bacterial burdens, reduced inflammatory responses, and fewer lung injuries in challenged mice hosts. Mechanistically, we found that Cys44 was a critical site for the full function of PA3880 in influencing alveolar macrophage phagocytosis and bacterial clearance. We also found that AnvM directly interacted with host receptors Toll-like receptor 2 (TLR2) and TLR5, which might lead to activation of the host immune response. Hence, we gave the name AnvM (anaerobic and virulence modulator) to the PA3880 protein. This characterization of AnvM could help to uncover new targets and strategies to treat P. aeruginosa infections. IMPORTANCE Infections by Pseudomonas aeruginosa, one of the most frequently isolated human pathogens, can create huge financial burdens. However, knowledge of the molecular mechanisms involved in the pathogenesis of P. aeruginosa remains elusive. We identified AnvM as a novel regulator of virulence in P. aeruginosa. Deletion of anvM altered the expression levels of more than 700 genes under aerobic and anaerobic conditions, including quorum sensing system genes and oxidative stress resistance genes. AnvM directly interacted with MvfR and Anr, thus regulating their downstream genes. More importantly, AnvM directly bound to TLR2 and TLR5, which turn on the host immune response. These findings provide insights into the significance of AnvM homologs in pathogenic bacteria and suggest a potential drug target against bacterial infection.

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