The CepIR quorum-sensing system contributes to the virulence of Burkholderia cenocepacia respiratory infections

Microbiology ◽  
2003 ◽  
Vol 149 (12) ◽  
pp. 3649-3658 ◽  
Author(s):  
P. A. Sokol ◽  
U. Sajjan ◽  
M. B. Visser ◽  
S. Gingues ◽  
J. Forstner ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Parent Strain ◽  
Respiratory Infections ◽  
Virulent Strain ◽  
Interleukin 1 ◽  
Homoserine Lactone ◽  
Burkholderia Cenocepacia ◽  
Sensing System ◽  
Quorum Sensing System ◽  
The Difference

The cepIR genes encode an N-acyl homoserine lactone (AHL)-dependent quorum-sensing system consisting of an AHL synthase that directs the synthesis of N-octanoyl-l-homoserine lactone (ohl) and n-hexanoyl-l-homoserine lactone and a transcriptional regulator. The virulence of cepIR mutants was examined in two animal models. Rats were infected with agar beads containing Burkholderia cenocepacia K56-2, K56-I2 (cepI : : Tpr) or K56-R2 (cepR : : Tn5-OT182). At 10 days post-infection, the extent of lung histopathological changes was significantly lower in lungs infected with K56-I2 or K56-R2 compared to the parent strain. Intranasal infections were performed in Cftr (−/−) mice and their wild-type siblings. K56-2 was more virulent in both groups of mice. K56-I2 was the least virulent strain and was not invasive in the Cftr (−/−) mice. OHL was readily detected in lung homogenates from Cftr (−/−) mice infected with K56-2 but was only detected at levels slightly above background in a few mice infected with K56-I2. Lung homogenates from mice infected with K56-2 had significantly higher levels of the inflammatory mediators murine macrophage inflammatory protein-2, KC/N51, interleukin-1β and interleukin-6 than those from K56-I2-infected animals. These studies indicate that a functional CepIR quorum-sensing system contributes to the severity of B. cenocepacia infections. A zinc metalloprotease gene (zmpA) was shown to be regulated by CepR and may be one of the factors that accounts for the difference in virulence between the cepI mutant and the parent strain.

scholarly journals Characterization of the cciIR Quorum-Sensing System in Burkholderia cenocepacia

2005 ◽  
Vol 73 (8) ◽  
pp. 4982-4992 ◽  
Author(s):  
Rebecca J. Malott ◽  
Adam Baldwin ◽  
Eshwar Mahenthiralingam ◽  
Pamela A. Sokol
Keyword(s):  
Quorum Sensing ◽  
Protease Activity ◽  
Parent Strain ◽  
Response Regulator ◽  
Homoserine Lactone ◽  
Burkholderia Cenocepacia ◽  
Pcr Analysis ◽  
Swarming Motility ◽  
Sensing System ◽  
Quorum Sensing System

ABSTRACT Several transmissible Burkholderia cenocepacia strains that infect multiple cystic fibrosis patients contain a genomic island designated as the cenocepacia island (cci). The cci contains a predicted N-acylhomoserine lactone (AHL) synthase gene, cciI, and a predicted response regulator gene, cciR. AHL production profiles indicated that CciI catalyzes the synthesis of N-hexanoyl-l-homoserine lactone and minor amounts of N-octanoyl-l-homoserine lactone. The cciI and cciR genes were found to be cotranscribed by reverse transcription-PCR analysis, and the expression of a cciIR::luxCDABE fusion in a cciR mutant suggested that the cciIR system negatively regulates its own expression. B. cenocepacia strains also have a cepIR quorum-sensing system. Expression of cepI::luxCDABE or cepR::luxCDABE fusions in a cciR mutant showed that CciR negatively regulates cepI but does not regulate cepR. Expression of the cciIR::luxCDABE fusion in a cepR mutant indicated that functional CepR is required for cciIR expression. Phylogenetic analysis suggested that the cciIR system was acquired by horizontal gene transfer from a distantly related organism and subsequently incorporated into the ancestral cepIR regulatory network. Mutations in cciI, cciR, cepI cciI, and cepR cciR were constructed in B. cenocepacia K56-2. The cciI mutant had greater protease activity and less swarming motility than the parent strain. The cciR mutant had less protease activity than the parent strain. The phenotypes of the cepI cciI and cepR cciR mutants were similar to cepI or cepR mutants, with less protease activity and swarming motility than the parent strain.

scholarly journals Inhibition of exoprotease production in Aeromonas hydrophila by rhizome extract of temu lawak (Curcuma xanthorrhiza (Roxb.)

2006 ◽  
Vol 4 (2) ◽  
pp. 45-54
Author(s):  
UMI LESTARI ◽  
ARTINI PANGASTUTI ◽  
ARI SUSILOWATI
Keyword(s):  
Quorum Sensing ◽  
Ethyl Acetate ◽  
Aeromonas Hydrophila ◽  
Ethanol Extract ◽  
Homoserine Lactone ◽  
Sensing System ◽  
Development Of Resistance ◽  
Quorum Sensing System ◽  
Assay Result ◽  
Curcuma Xanthorrhiza

Conventional treatment of infectious diseases is based on compounds that kill or inhibit the growth of bacteria. A major concern with this approach is the frequent development of resistance to antimicrobial compounds. The discovery of communication (quorum sensing system) regulating bacterial virulence opens up ways to control certain bacterial infectious without interfering the growth. The fish pathogen Aeromonas hydrophila produces quorum sensing signal, NButanoyl-L-Homoserine Lactone (C4-HSL). C4-HSL regulates exoprotease synthesis, a virulence factor of A. hydrophila. Expression of exoprotease can be blocked by using quorum sensing inhibitor. The purpose of this study was to investigate the inhibiting effect of Curcuma xanthorrhiza (Roxb.) extract to exoprotease production of A. hydrophila. Extraction was conducted by using n-hexane, ethyl acetate and ethanol. The qualitative exoprotease assay result showed that n-hexane extract of C. xanthorrhiza had not effect on growth and exoprotease production of A. hydrophila. Meanwhile, 4% of ethyl acetate and ethanol extract of C. xanthorrhiza can inhibit exoprotease production without affecting A. hydrophilla growth. The quantitative exoprotease assay result showed that 4% of ethyl acetate and ethanol extract can inhibit the exoprotease production by 93,9% and 95,6%. The growth of A. hydrophila was not affected by this extract.

scholarly journals PqsE Functions Independently of PqsR-Pseudomonas Quinolone Signal and Enhances the rhl Quorum-Sensing System

2008 ◽  
Vol 190 (21) ◽  
pp. 7043-7051 ◽  
Author(s):  
John M. Farrow ◽  
Zoe M. Sund ◽  
Matthew L. Ellison ◽  
Dana S. Wade ◽  
James P. Coleman ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Virulence Factors ◽  
Opportunistic Pathogen ◽  
Homoserine Lactone ◽  
Chronic Infections ◽  
Signaling Systems ◽  
Sensing System ◽  
Pseudomonas Quinolone Signal ◽  
Quorum Sensing System ◽  
Hostile Environments

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.

scholarly journals The LuxM Homologue VanM from Vibrio anguillarumDirects the Synthesis of N-(3-Hydroxyhexanoyl)homoserine Lactone and N-Hexanoylhomoserine Lactone

2001 ◽  
Vol 183 (12) ◽  
pp. 3537-3547 ◽  
Author(s):  
Debra L. Milton ◽  
Victoria J. Chalker ◽  
David Kirke ◽  
Andrea Hardman ◽  
Miguel Cámara ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Vibrio Anguillarum ◽  
Homoserine Lactone ◽  
Regulatory Elements ◽  
Sequencing Error ◽  
Infection Model ◽  
Reading Frame ◽  
Acylhomoserine Lactone ◽  
Sensing System ◽  
Quorum Sensing System

ABSTRACT Vibrio anguillarum, which causes terminal hemorrhagic septicemia in fish, was previously shown to possess a LuxRI-type quorum-sensing system (vanRI) and to produceN-(3-oxodecanoyl)homoserine lactone (3-oxo-C10-HSL). However, a vanI null mutant still activatedN-acylhomoserine lactone (AHL) biosensors, indicating the presence of an additional quorum-sensing circuit in V. anguillarum. In this study, we have characterized this second system. Using high-pressure liquid chromatography in conjunction with mass spectrometry and chemical analysis, we identified two additional AHLs as N-hexanoylhomoserine lactone (C6-HSL) andN-(3-hydroxyhexanoyl)homoserine lactone (3-hydroxy-C6-HSL). Quantification of each AHL present in stationary-phase V. anguillarum spent culture supernatants indicated that 3-oxo-C10-HSL, 3-hydroxy-C6-HSL, and C6-HSL are present at approximately 8.5, 9.5, and 0.3 nM, respectively. Furthermore,vanM, the gene responsible for the synthesis of these AHLs, was characterized and shown to be homologous to the luxLand luxM genes, which are required for the production ofN-(3-hydroxybutanoyl)homoserine lactone in Vibrio harveyi. However, resequencing of the V. harveyi luxL/luxM junction revealed a sequencing error present in the published sequence, which when corrected resulted in a single open reading frame (termed luxM). Downstream ofvanM, we identified a homologue of luxN(vanN) that encodes a hybrid sensor kinase which forms part of a phosphorelay cascade involved in the regulation of bioluminescence in V. harveyi. A mutation in vanM abolished the production of C6-HSL and 3-hydroxy-C6-HSL. In addition, production of 3-oxo-C10-HSL was abolished in the vanM mutant, suggesting that 3-hydroxy-C6-HSL and C6-HSL regulate the production of 3-oxo-C10-HSL via vanRI. However, a vanN mutant displayed a wild-type AHL profile. Neither mutation affected either the production of proteases or virulence in a fish infection model. These data indicate that V. anguillarum possesses a hierarchical quorum sensing system consisting of regulatory elements homologous to those found in both V. fischeri (the LuxRI homologues VanRI) and V. harveyi (the LuxMN homologues, VanMN).

scholarly journals The Plant Pathogen Pantoea ananatis Produces N-Acylhomoserine Lactone and Causes Center Rot Disease of Onion by Quorum Sensing

2007 ◽  
Vol 189 (22) ◽  
pp. 8333-8338 ◽  
Author(s):  
Tomohiro Morohoshi ◽  
Yuta Nakamura ◽  
Go Yamazaki ◽  
Akio Ishida ◽  
Norihiro Kato ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Biofilm Formation ◽  
Receptor Gene ◽  
Homoserine Lactone ◽  
Pantoea Ananatis ◽  
Signal Molecule ◽  
Acylhomoserine Lactone ◽  
Sensing System ◽  
Quorum Sensing System ◽  
Rot Disease

ABSTRACT A number of gram-negative bacteria have a quorum-sensing system and produce N-acyl-l-homoserine lactone (AHL) that they use them as a quorum-sensing signal molecule. Pantoea ananatis is reported as a common colonist of wheat heads at ripening and causes center rot of onion. In this study, we demonstrated that P. ananatis SK-1 produced two AHLs, N-hexanoyl-l-homoserine lactone (C6-HSL) and N-(3-oxohexanoyl)-l-homoserine lactone (3-oxo-C6-HSL). We cloned the AHL-synthase gene (eanI) and AHL-receptor gene (eanR) and revealed that the deduced amino acid sequence of EanI/EanR showed high identity to those of EsaI/EsaR from P. stewartii. EanR repressed the ean box sequence and the addition of AHLs resulted in derepression of ean box. Inactivation of the chromosomal eanI gene in SK-1 caused disruption of exopolysaccharide (EPS) biosynthesis, biofilm formation, and infection of onion leaves, which were recovered by adding exogenous 3-oxo-C6-HSL. These results demonstrated that the quorum-sensing system involved the biosynthesis of EPS, biofilm formation, and infection of onion leaves in P. ananatis SK-1.

scholarly journals N-Acyl-l-Homoserine Lactone-Mediated Regulation of the Lip Secretion System inSerratia liquefaciens MG1

2001 ◽  
Vol 183 (5) ◽  
pp. 1805-1809 ◽  
Author(s):  
Kathrin Riedel ◽  
Thomas Ohnesorg ◽  
Karen A. Krogfelt ◽  
Thomas S. Hansen ◽  
Kenji Omori ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Homoserine Lactone ◽  
Secretion System ◽  
Type I ◽  
Extracellular Lipase ◽  
Sensing System ◽  
Serratia Liquefaciens ◽  
Quorum Sensing System ◽  
Insertion Mutants

ABSTRACT The analysis of Serratia liquefaciens MG1 ′luxAB insertion mutants that are responsive toN-butanoyl-l-homoserine lactone revealed that expression of lipB is controlled by the swrquorum-sensing system. LipB is part of the Lip exporter, a type I secretion system, which is responsible for the secretion of extracellular lipase, metalloprotease, and S-layer protein.

scholarly journals N-Octanoylhomoserine lactone signalling mediated by the BpsI–BpsR quorum sensing system plays a major role in biofilm formation of Burkholderia pseudomallei

Microbiology ◽  
2011 ◽  
Vol 157 (4) ◽  
pp. 1176-1186 ◽  
Author(s):  
Akshamal Mihiranga Gamage ◽  
Guanghou Shui ◽  
Markus R. Wenk ◽  
Kim Lee Chua
Keyword(s):  
Quorum Sensing ◽  
Biofilm Formation ◽  
Burkholderia Pseudomallei ◽  
Homoserine Lactone ◽  
Tandem Ms ◽  
Wild Type ◽  
Acylhomoserine Lactone ◽  
Sensing System ◽  
Sensing Systems ◽  
Quorum Sensing System

The genome of Burkholderia pseudomallei encodes three acylhomoserine lactone (AHL) quorum sensing systems, each comprising an AHL synthase and a signal receptor/regulator. The BpsI–BpsR system produces N-octanoylhomoserine lactone (C8HL) and is positively auto-regulated by its AHL product. The products of the remaining two systems have not been identified. In this study, tandem MS was used to identify and quantify the AHL species produced by three clinical B. pseudomallei isolates – KHW, K96243 and H11 – three isogenic KHW mutants that each contain a null mutation in an AHL synthase gene, and recombinant Escherichia coli heterologously expressing each of the three B. pseudomallei AHL synthase genes. BpsI synthesized predominantly C8HL, which accounted for more than 95 % of the extracellular AHLs produced in stationary-phase KHW cultures. The major products of BpsI2 and BpsI3 were N-(3-hydroxy-octanoyl)homoserine lactone (OHC8HL) and N-(3-hydroxy-decanoyl)homoserine lactone, respectively, and their corresponding transcriptional regulators, BpsR2 and BpsR3, were capable of driving reporter gene expression in the presence of these cognate lactones. Formation of biofilm by B. pseudomallei KHW was severely impaired in mutants lacking either BpsI or BpsR but could be restored to near wild-type levels by exogenous C8HL. BpsI2 was not required, and BpsI3 was partially required for biofilm formation. Unlike the bpsI mutant, biofilm formation in the bpsI3 mutant could not be restored to wild-type levels in the presence of OHC8HL, the product of BpsI3. C8HL and OHC8HL had opposite effects on biofilm formation; exogenous C8HL enhanced biofilm formation in both the bpsI3 mutant and wild-type KHW while exogenous OHC8HL suppressed the formation of biofilm in the same strains. We propose that exogenous OHC8HL antagonizes biofilm formation in B. pseudomallei, possibly by competing with endogenous C8HL for binding to BpsR.

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