Production of N-acyl-?-homoserine lactones by P. aeruginosa isolates from chronic lung infections associated with cystic fibrosis

Geisenberger, O

doi:10.1016/s0378-1097(00)00059-8

Cited by 40 publications

(62 citation statements)

References 15 publications

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“…In a first step to assess the possibility of AHL-mediated intergeneric signalling between P. aeruginosa and B. cepacia we determined the AHL profiles of bacterial isolates from one CF patient who became co-infected with B. cepacia (Geisenberger et al, 2000). P. aeruginosa SH1, a strain that was isolated from the patient prior to co-infection with B. cepacia, produced large amounts of AHL molecules.…”

Section: Ahl Profiles Of Strains Used In This Studymentioning

confidence: 99%

“…On the basis of their mobilities (R F values) and by including appropriate reference compounds it was concluded that these molecules represent 3-oxo-C12-HSL, 3-oxo-C8-HSL, 3-oxo-C14-HSL, C6-HSL and C8-HSL ( Fig. 2 ; Geisenberger et al, 2000). As a control we also included the well-characterized P. aeruginosa strain PAO1 in this analysis.…”

Section: Ahl Profiles Of Strains Used In This Studymentioning

confidence: 99%

“…However, C4-HSL could not be detected by the aid of plasmid pSB403 since this AHL sensor is very insensitive to this signal molecule (Winson et al, 1998). The production of both C4-HSL and C6-HSL was easily visualized by the use of Chromobacterium violaceum CV026 as sensor (Geisenberger et al, 2000). This sensor is highly sensitive to unsubstituted short-chain AHL molecules but is quite insensitive to other AHLs (McClean et al, 1997).…”

Section: Ahl Profiles Of Strains Used In This Studymentioning

confidence: 99%

“…the types and amounts of AHL molecules, of sequential P. aeruginosa isolates from several chronically infected CF patients by TLC (Geisenberger et al, 2000). In one case the patient became transiently co-infected with an AHLproducing B. cepacia strain.…”

Section: Introductionmentioning

confidence: 99%

“…of 1n0) and separated by TLC as described by Geisenberger et al (2000). The AHL molecules were visualized by overlaying the TLC plates with soft agar seeded with the sensor strain E. coli MT102(pSB403) (Winson et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

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N-Acylhomoserine-lactone-mediated communication between Pseudomonas aeruginosa and Burkholderia cepacia in mixed biofilms

Riedel¹,

Hentzer²,

et al. 2001

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Pseudomonas aeruginosa and Burkholderia cepacia are capable of forming mixed biofilms in the lungs of cystic fibrosis patients. Both bacteria employ quorum-sensing systems, which rely on N-acylhomoserine lactone (AHL) signal molecules, to co-ordinate expression of virulence factors with the formation of biofilms. As both bacteria utilize the same class of signal molecules the authors investigated whether communication between the species occurs. To address this issue, novel Gfp-based biosensors for non-destructive, in situ detection of AHLs were constructed and characterized. These sensors were used to visualize AHL-mediated communication in mixed biofilms, which were cultivated either in artificial flow chambers or in alginate beads in mouse lung tissue. In both model systems B. cepacia was capable of perceiving the AHL signals produced by P. aeruginosa, while the latter strain did not respond to the molecules produced by B. cepacia. Measurements of extracellular proteolytic activities of defined quorum-sensing mutants grown in media complemented with AHL extracts prepared from culture supernatants of various wild-type and mutant strains supported the view of unidirectional signalling between the two strains.

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Section: Ahl Profiles Of Strains Used In This Studymentioning

confidence: 99%

Section: Ahl Profiles Of Strains Used In This Studymentioning

confidence: 99%

Section: Ahl Profiles Of Strains Used In This Studymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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N-Acylhomoserine-lactone-mediated communication between Pseudomonas aeruginosa and Burkholderia cepacia in mixed biofilms

Riedel¹,

Hentzer²,

et al. 2001

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Serum influences the expression of Pseudomonas aeruginosa quorum‐sensing genes and QS‐controlled virulence genes during early and late stages of growth

et al. 2013

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In response to diverse environmental stimuli at different infection sites, Pseudomonas aeruginosa, a serious nosocomial pathogen, coordinates the production of different virulence factors through a complicated network of the hierarchical quorum-sensing (QS) systems including the las, rhl, and the 2-alkyl-4-quinolone-related QS systems. We recently showed that at early stages of growth serum alters the expression of numerous P. aeruginosa genes. In this study, we utilized transcriptional analysis and enzyme assays to examine the effect of serum on the QS and QS-controlled virulence factors during early and late phases of growth of the P. aeruginosa strain PAO1. At early phase, serum repressed the transcription of lasI, rhlI, and pqsA but not lasR or rhlR. However, at late phase, serum enhanced the expression of all QS genes. Serum produced a similar effect on the synthesis of the autoinducers 3OC12-HSL, C4-HSL, and HHQ/PQS. Additionally, serum repressed the expression of several QS-controlled genes in the early phase, but enhanced them in the late phase. Furthermore, serum influenced the expression of different QS-positive (vqsR, gacA, and vfr) as well as QS-negative (rpoN, qscR, mvaT, and rsmA) regulatory genes at either early or late phases of growth. However, with the exception of PAOΔvfr, we detected comparable levels of lasI/lasR expression in PAO1 and PAO1 mutants defective in these regulatory genes. At late stationary phase, serum failed to enhance lasI/lasR expression in PAOΔvfr. These results suggest that depending on the phase of growth, serum differentially influenced the expression of P. aeruginosa QS and QS-controlled virulence genes. In late phase, serum enhanced the expression of las genes through vfr.

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Burkholderia cenocepacia utilizes a type VI secretion system for bacterial competition

et al. 2019

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Burkholderia cenocepacia is an opportunistic bacterial pathogen that poses a significant threat to individuals with cystic fibrosis by provoking a strong inflammatory response within the lung. It possesses a type VI secretion system (T6SS), a secretory apparatus that can perforate the cellular membrane of other bacterial species and/or eukaryotic targets, to deliver an arsenal of effector proteins. The B. cenocepacia T6SS (T6SS‐1) has been shown to be implicated in virulence in rats and contributes toward actin rearrangements and inflammasome activation in B. cenocepacia ‐infected macrophages. Here, we present bioinformatics evidence to suggest that T6SS‐1 is the archetype T6SS in the Burkholderia genus. We show that B. cenocepacia T6SS‐1 is active under normal laboratory growth conditions and displays antibacterial activity against other Gram‐negative bacterial species. Moreover, B. cenocepacia T6SS‐1 is not required for virulence in three eukaryotic infection models. Bioinformatics analysis identified several candidate T6SS‐dependent effectors that may play a role in the antibacterial activity of B. cenocepacia T6SS‐1. We conclude that B. cenocepacia T6SS‐1 plays an important role in bacterial competition for this organism, and probably in all Burkholderia species that possess this system, thereby broadening the range of species that utilize the T6SS for this purpose.

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Production of N-acyl-?-homoserine lactones by P. aeruginosa isolates from chronic lung infections associated with cystic fibrosis

Cited by 40 publications

References 15 publications

N-Acylhomoserine-lactone-mediated communication between Pseudomonas aeruginosa and Burkholderia cepacia in mixed biofilms

N-Acylhomoserine-lactone-mediated communication between Pseudomonas aeruginosa and Burkholderia cepacia in mixed biofilms

Serum influences the expression of Pseudomonas aeruginosa quorum‐sensing genes and QS‐controlled virulence genes during early and late stages of growth

Burkholderia cenocepacia utilizes a type VI secretion system for bacterial competition

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