Exogenous Yersinia pestis quorum sensing molecules N-octanoyl-homoserine lactone and N-(3-oxooctanoyl)-homoserine lactone regulate the LcrV virulence factor

2009 ◽  
Vol 46 (5) ◽  
pp. 283-287 ◽  
Author(s):  
H. Carl Gelhaus ◽  
David A. Rozak ◽  
William C. Nierman ◽  
Dan Chen ◽  
John J. Varga, Mojgan Zadeh ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Yersinia Pestis ◽  
Virulence Factor ◽  
Homoserine Lactone

scholarly journals Quorum Sensing: a Transcriptional Regulatory System Involved in the Pathogenicity of Burkholderia mallei

2004 ◽  
Vol 72 (11) ◽  
pp. 6589-6596 ◽  
Author(s):  
Ricky L. Ulrich ◽  
David DeShazer ◽  
Harry B. Hines ◽  
Jeffrey A. Jeddeloh
Keyword(s):  
Quorum Sensing ◽  
Virulence Factor ◽  
Regulatory System ◽  
In Silico Analysis ◽  
Homoserine Lactone ◽  
Burkholderia Mallei ◽  
Wild Type ◽  
Transcriptional Regulatory ◽  
A Cell

ABSTRACT Numerous gram-negative bacterial pathogens regulate virulence factor expression by using a cell density mechanism termed quorum sensing (QS). An in silico analysis of the Burkholderia mallei ATCC 23344 genome revealed that it encodes at least two luxI and four luxR homologues. Using mass spectrometry, we showed that wild-type B. mallei produces the signaling molecules N-octanoyl-homoserine lactone and N-decanoyl-homoserine lactone. To determine if QS is involved in the virulence of B. mallei, we generated mutations in each putative luxIR homologue and tested the pathogenicities of the derivative strains in aerosol BALB/c mouse and intraperitoneal hamster models. Disruption of the B. mallei QS alleles, especially in RJ16 (bmaII) and RJ17 (bmaI3), which are luxI mutants, significantly reduced virulence, as indicated by the survival of mice who were aerosolized with 104 CFU (10 50% lethal doses [LD50s]). For the B. mallei transcriptional regulator mutants (luxR homologues), mutation of the bmaR5 allele resulted in the most pronounced decrease in virulence, with 100% of the challenged animals surviving a dose of 10 LD50s. Using a Syrian hamster intraperitoneal model of infection, we determined the LD50s for wild-type B. mallei and each QS mutant. An increase in the relative LD50 was found for RJ16 (bmaI1) (>967 CFU), RJ17 (bmaI3) (115 CFU), and RJ20 (bmaR5) (151 CFU) compared to wild-type B. mallei (<13 CFU). These findings demonstrate that B. mallei carries multiple luxIR homologues that either directly or indirectly regulate the biosynthesis of an essential virulence factor(s) that contributes to the pathogenicity of B. mallei in vivo.

scholarly journals Effects of Antibiotics on Quorum Sensing in Pseudomonas aeruginosa

2008 ◽  
Vol 52 (10) ◽  
pp. 3648-3663 ◽  
Author(s):  
Mette E. Skindersoe ◽  
Morten Alhede ◽  
Richard Phipps ◽  
Liang Yang ◽  
Peter O. Jensen ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Virulence Factor ◽  
Dna Microarrays ◽  
Underlying Mechanism ◽  
Homoserine Lactone ◽  
Reverse Transcription Pcr ◽  
Animal Infection ◽  
Beneficial Action ◽  
Severe Infections

ABSTRACT During infection, Pseudomonas aeruginosa employs bacterial communication (quorum sensing [QS]) to coordinate the expression of tissue-damaging factors. QS-controlled gene expression plays a pivotal role in the virulence of P. aeruginosa, and QS-deficient mutants cause less severe infections in animal infection models. Treatment of cystic fibrosis (CF) patients chronically infected with P. aeruginosa with the macrolide antibiotic azithromycin (AZM) has been demonstrated to improve the clinical outcome. Several studies indicate that AZM may accomplish its beneficial action in CF patients by impeding QS, thereby reducing the pathogenicity of P. aeruginosa. This led us to investigate whether QS inhibition is a common feature of antibiotics. We present the results of a screening of 12 antibiotics for their QS-inhibitory activities using a previously described QS inhibitor selector 1 strain. Three of the antibiotics tested, AZM, ceftazidime (CFT), and ciprofloxacin (CPR), were very active in the assay and were further examined for their effects on QS-regulated virulence factor production in P. aeruginosa. The effects of the three antibiotics administered at subinhibitory concentrations were investigated by use of DNA microarrays. Consistent results from the virulence factor assays, reverse transcription-PCR, and the DNA microarrays support the finding that AZM, CFT, and CPR decrease the expression of a range of QS-regulated virulence factors. The data suggest that the underlying mechanism may be mediated by changes in membrane permeability, thereby influencing the flux of N-3-oxo-dodecanoyl-l-homoserine lactone.

scholarly journals Transcriptome Analysis of Acetyl-Homoserine Lactone-Based Quorum Sensing Regulation in Yersinia pestis

PLoS ONE ◽  
2013 ◽  
Vol 8 (4) ◽  
pp. e62337 ◽  
Author(s):  
Christopher N. LaRock ◽  
Jing Yu ◽  
Alexander R. Horswill ◽  
Matthew R. Parsek ◽  
F. Chris Minion
Keyword(s):  
Quorum Sensing ◽  
Yersinia Pestis ◽  
Transcriptome Analysis ◽  
Homoserine Lactone

scholarly journals Correction: Transcriptome Analysis of Acetyl-Homoserine Lactone-Based Quorum Sensing Regulation in Yersinia pestis

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
Author(s):  
Christopher N. LaRock ◽  
Jing Yu ◽  
Alexander R. Horswill ◽  
Matthew R. Parsek ◽  
F. Chris Minion
Keyword(s):  
Quorum Sensing ◽  
Yersinia Pestis ◽  
Transcriptome Analysis ◽  
Homoserine Lactone

scholarly journals The BpeAB-OprB Efflux Pump of Burkholderia pseudomallei 1026b Does Not Play a Role in Quorum Sensing, Virulence Factor Production, or Extrusion of Aminoglycosides but Is a Broad-Spectrum Drug Efflux System

2010 ◽  
Vol 54 (8) ◽  
pp. 3113-3120 ◽  
Author(s):  
Takehiko Mima ◽  
Herbert P. Schweizer
Keyword(s):  
Quorum Sensing ◽  
Virulence Factor ◽  
Burkholderia Pseudomallei ◽  
Efflux Pump ◽  
Homoserine Lactone ◽  
Genetically Engineered ◽  
Multidrug Efflux ◽  
Efflux System ◽  
Aminoglycoside Resistance

ABSTRACT Most Burkholderia pseudomallei strains are intrinsically aminoglycoside resistant, mainly due to AmrAB-OprA-mediated efflux. Rare naturally occurring or genetically engineered mutants lacking this pump are aminoglycoside susceptible despite the fact that they also encode and express BpeAB-OprB, which was reported to mediate efflux of aminoglycosides in the Singapore strain KHW. To reassess the role of BpeAB-OprB in B. pseudomallei aminoglycoside resistance, we used mutants overexpressing or lacking this pump in either AmrAB-OprA-proficient or -deficient strain 1026b backgrounds. Our data show that BpeAB-OprB does not mediate efflux of aminoglycosides but is a multidrug efflux system which extrudes macrolides, fluoroquinolones, tetracyclines, acriflavine, and, to a lesser extent, chloramphenicol. Phylogenetically, BpeAB-OprB is closely related to Pseudomonas aeruginosa MexAB-OprM, which has a similar substrate spectrum. AmrAB-OprA is most closely related to MexXY, the only P. aeruginosa efflux pump known to extrude aminoglycosides. Since BpeAB-OprB in strain KHW was also implicated in playing a major role in export of acylated homoserine lactone (AHL) quorum-sensing molecules and in expression of diverse virulence factors, we explored whether this was also true in the strain 1026b background. The results showed that BpeAB-OprB was not required for AHL export, and mutants lacking this efflux system exhibited normal swimming motility and siderophore production, which were severely impaired in KHW bpeAB-oprB mutants. Biofilm formation was impaired in 1026b Δ(amrRAB-oprA) and Δ(amrRAB-oprA) Δ(bpeAB-oprB) mutants. At present, we do not know why our BpeAB-OprB susceptibility and virulence factor expression results with 1026b and its derivatives are different from those previously published for Singapore strain KHW.

scholarly journals Quorum sensing regulation in Erwinia carotovora affects development of Drosophila melanogaster infected larvae

2019 ◽  
Author(s):  
Filipe J. D. Vieira ◽  
Pol Nadal-Jimenez ◽  
Luis Teixeira ◽  
Karina B. Xavier
Keyword(s):  
Drosophila Melanogaster ◽  
Quorum Sensing ◽  
Developmental Delay ◽  
Virulence Factors ◽  
Virulence Factor ◽  
Plant Cell Wall ◽  
Erwinia Carotovora ◽  
Homoserine Lactone ◽  
Pectolytic Enzymes ◽  
Two Component

AbstractMulti-host bacteria must rapidly adapt to drastic environmental changes, relying on integration of multiple stimuli for an optimal genetic response. Erwinia spp. are phytopathogens that cause soft-rot disease in plants. Erwinia carotovora Ecc15 is used as a model for bacterial oral-route infection in Drosophila melanogaster as it harbors a gene, the Erwinia virulence factor (Evf), which has been previously shown to be a major determinant for infection of D. melanogaster gut. However, the factors involved in regulation of evf expression are poorly understood. We investigated whether evf could be controlled by quorum sensing since, in the Erwinia genus, quorum sensing regulates pectolytic enzymes, the major virulence factors needed to infect plants. Here, we show that transcription of evf is positively regulated by quorum sensing in Ecc15 via the acyl-homoserine lactone (AHL) signal synthase ExpI, and the AHL receptors ExpR1 and ExpR2. Moreover, we demonstrate that the GacS/A two-component system is partially required for evf expression. We also show that the load of Ecc15 in the gut depends upon the quorum sensing-mediated regulation of evf. Furthermore, we demonstrate that larvae infected with Ecc15 suffer a developmental delay as a direct consequence of the regulation of evf via quorum sensing. Overall, our results show that Ecc15 relies on quorum sensing to control production of both pectolytic enzymes and Evf. This regulation influences the interaction of Ecc15 with its two known hosts, indicating that quorum sensing and GacS/A signaling systems may impact bacterial dissemination via insect vectors that feed on rotting plants.SignificanceIntegration of genetic networks allows bacteria to rapidly adapt to changing environments. This is particularly important in bacteria that interact with multiple hosts. Erwinia carotovora Ecc15 is a plant pathogen that uses Drosophila melanogaster as a vector. To interact with these two hosts, Ecc15 uses two different sets of virulence factors: plant cell wall-degrading enzymes to infect plants and the Erwinia virulence factor (evf) to infect Drosophila. Our work shows that, despite the virulence factors being different, both are regulated by homoserine lactone quorum sensing and the two component GacS/A system. Moreover, we show that these pathways are essential for Ecc15 loads in the gut of Drosophila and that this interaction carries a cost to the vector in the form of a developmental delay. Our findings provide evidence for the importance of quorum sensing regulation in the establishment of multi-host interactions.

scholarly journals Involvement of a Quorum-Sensing-Regulated Lipase Secreted by a Clinical Isolate of Burkholderia glumae in Severe Disease Symptoms in Rice

2007 ◽  
Vol 73 (15) ◽  
pp. 4950-4958 ◽  
Author(s):  
Giulia Devescovi ◽  
Joseph Bigirimana ◽  
Giuliano Degrassi ◽  
Laura Cabrio ◽  
John J. LiPuma ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Clinical Isolate ◽  
Virulence Factor ◽  
Spontaneous Mutation ◽  
Severe Disease ◽  
Homoserine Lactone ◽  
Strain Atcc ◽  
Human Pathogens ◽  
Burkholderia Glumae ◽  
Important Virulence Factor

ABSTRACT Burkholderia glumae is an emerging rice pathogen in several areas around the world. Closely related Burkholderia species are important opportunistic human pathogens for specific groups of patients, such as patients with cystic fibrosis and patients with chronic granulomatous disease. Here we report that the first clinical isolate of B. glumae, strain AU6208, has retained its capability to be very pathogenic to rice. As previously reported for rice isolate B. glumae BGR1 (and also for the clinical isolate AU6208), TofI or TofR acyl homoserine lactone (AHL) quorum sensing played a pivotal role in rice virulence. We report that AHL quorum sensing in B. glumae AU6208 regulates secreted LipA lipase and toxoflavin, the phytotoxin produced by B. glumae. B. glumae AU6208 lipA mutants were no longer pathogenic to rice, indicating that the lipase is an important virulence factor. It was also established that type strain B. glumae ATCC 33617 did not produce toxoflavin and lipase and was nonpathogenic to rice. It was determined that in strain ATCC 33617 the LuxR family quorum-sensing sensor/regulator TofR was inactive. Introducing the tofR gene of B. glumae AU6208 in strain ATCC 33617 restored its ability to produce toxoflavin and the LipA lipase. This study extends the role of AHL quorum sensing in rice pathogenicity through the regulation of a lipase which was demonstrated to be a virulence factor. It is the first report of a clinical B. glumae isolate retaining strong rice pathogenicity and finally determined that B. glumae can undergo phenotypic conversion through a spontaneous mutation in the tofR regulator.

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