Quorum sensing and virulence of Pseudomonas aeruginosa during lung infection of cystic fibrosis patients

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Quorum sensing and virulence of Pseudomonas aeruginosa during lung infection of cystic fibrosis patients. / Bjarnsholt, Thomas; Jensen, Peter Østrup; Jakobsen, Tim Holm; Phipps, Richard; Nielsen, Anne Kirstine; Rybtke, Morten Theil; Tolker-Nielsen, Tim; Givskov, Michael; Høiby, Niels; Ciofu, Oana; Scandinavian Cystic Fibrosis Study Consortium.

In: PLoS ONE, Vol. 5, No. 4, 01.01.2010, p. e10115.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Bjarnsholt, T, Jensen, PØ, Jakobsen, TH, Phipps, R, Nielsen, AK, Rybtke, MT, Tolker-Nielsen, T, Givskov, M, Høiby, N, Ciofu, O & Scandinavian Cystic Fibrosis Study Consortium 2010, 'Quorum sensing and virulence of Pseudomonas aeruginosa during lung infection of cystic fibrosis patients', PLoS ONE, vol. 5, no. 4, pp. e10115. https://doi.org/10.1371/journal.pone.0010115

APA

Bjarnsholt, T., Jensen, P. Ø., Jakobsen, T. H., Phipps, R., Nielsen, A. K., Rybtke, M. T., Tolker-Nielsen, T., Givskov, M., Høiby, N., Ciofu, O., & Scandinavian Cystic Fibrosis Study Consortium (2010). Quorum sensing and virulence of Pseudomonas aeruginosa during lung infection of cystic fibrosis patients. PLoS ONE, 5(4), e10115. https://doi.org/10.1371/journal.pone.0010115

Vancouver

Bjarnsholt T, Jensen PØ, Jakobsen TH, Phipps R, Nielsen AK, Rybtke MT et al. Quorum sensing and virulence of Pseudomonas aeruginosa during lung infection of cystic fibrosis patients. PLoS ONE. 2010 Jan 1;5(4):e10115. https://doi.org/10.1371/journal.pone.0010115

Author

Bjarnsholt, Thomas ; Jensen, Peter Østrup ; Jakobsen, Tim Holm ; Phipps, Richard ; Nielsen, Anne Kirstine ; Rybtke, Morten Theil ; Tolker-Nielsen, Tim ; Givskov, Michael ; Høiby, Niels ; Ciofu, Oana ; Scandinavian Cystic Fibrosis Study Consortium. / Quorum sensing and virulence of Pseudomonas aeruginosa during lung infection of cystic fibrosis patients. In: PLoS ONE. 2010 ; Vol. 5, No. 4. pp. e10115.

Bibtex

@article{872e24807d2e11df928f000ea68e967b,
title = "Quorum sensing and virulence of Pseudomonas aeruginosa during lung infection of cystic fibrosis patients",
abstract = "Pseudomonas aeruginosa is the predominant microorganism in chronic lung infection of cystic fibrosis patients. The chronic lung infection is preceded by intermittent colonization. When the chronic infection becomes established, it is well accepted that the isolated strains differ phenotypically from the intermittent strains. Dominating changes are the switch to mucoidity (alginate overproduction) and loss of epigenetic regulation of virulence such as the Quorum Sensing (QS). To elucidate the dynamics of P. aeruginosa QS systems during long term infection of the CF lung, we have investigated 238 isolates obtained from 152 CF patients at different stages of infection ranging from intermittent to late chronic. Isolates were characterized with regard to QS signal molecules, alginate, rhamnolipid and elastase production and mutant frequency. The genetic basis for change in QS regulation were investigated and identified by sequence analysis of lasR, rhlR, lasI and rhlI. The first QS system to be lost was the one encoded by las system 12 years (median value) after the onset of the lung infection with subsequent loss of the rhl encoded system after 17 years (median value) shown as deficiencies in production of the 3-oxo-C12-HSL and C4-HSL QS signal molecules respectively. The concomitant development of QS malfunction significantly correlated with the reduced production of rhamnolipids and elastase and with the occurrence of mutations in the regulatory genes lasR and rhlR. Accumulation of mutations in both lasR and rhlR correlated with development of hypermutability. Interestingly, a higher number of mucoid isolates were found to produce C4-HSL signal molecules and rhamnolipids compared to the non-mucoid isolates. As seen from the present data, we can conclude that P. aeruginosa and particularly the mucoid strains do not lose the QS regulation or the ability to produce rhamnolipids until the late stage of the chronic infection.",
author = "Thomas Bjarnsholt and Jensen, {Peter {\O}strup} and Jakobsen, {Tim Holm} and Richard Phipps and Nielsen, {Anne Kirstine} and Rybtke, {Morten Theil} and Tim Tolker-Nielsen and Michael Givskov and Niels H{\o}iby and Oana Ciofu and {Scandinavian Cystic Fibrosis Study Consortium}",
year = "2010",
month = jan,
day = "1",
doi = "10.1371/journal.pone.0010115",
language = "English",
volume = "5",
pages = "e10115",
journal = "PLoS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "4",

}

RIS

TY - JOUR

T1 - Quorum sensing and virulence of Pseudomonas aeruginosa during lung infection of cystic fibrosis patients

AU - Bjarnsholt, Thomas

AU - Jensen, Peter Østrup

AU - Jakobsen, Tim Holm

AU - Phipps, Richard

AU - Nielsen, Anne Kirstine

AU - Rybtke, Morten Theil

AU - Tolker-Nielsen, Tim

AU - Givskov, Michael

AU - Høiby, Niels

AU - Ciofu, Oana

AU - Scandinavian Cystic Fibrosis Study Consortium

PY - 2010/1/1

Y1 - 2010/1/1

N2 - Pseudomonas aeruginosa is the predominant microorganism in chronic lung infection of cystic fibrosis patients. The chronic lung infection is preceded by intermittent colonization. When the chronic infection becomes established, it is well accepted that the isolated strains differ phenotypically from the intermittent strains. Dominating changes are the switch to mucoidity (alginate overproduction) and loss of epigenetic regulation of virulence such as the Quorum Sensing (QS). To elucidate the dynamics of P. aeruginosa QS systems during long term infection of the CF lung, we have investigated 238 isolates obtained from 152 CF patients at different stages of infection ranging from intermittent to late chronic. Isolates were characterized with regard to QS signal molecules, alginate, rhamnolipid and elastase production and mutant frequency. The genetic basis for change in QS regulation were investigated and identified by sequence analysis of lasR, rhlR, lasI and rhlI. The first QS system to be lost was the one encoded by las system 12 years (median value) after the onset of the lung infection with subsequent loss of the rhl encoded system after 17 years (median value) shown as deficiencies in production of the 3-oxo-C12-HSL and C4-HSL QS signal molecules respectively. The concomitant development of QS malfunction significantly correlated with the reduced production of rhamnolipids and elastase and with the occurrence of mutations in the regulatory genes lasR and rhlR. Accumulation of mutations in both lasR and rhlR correlated with development of hypermutability. Interestingly, a higher number of mucoid isolates were found to produce C4-HSL signal molecules and rhamnolipids compared to the non-mucoid isolates. As seen from the present data, we can conclude that P. aeruginosa and particularly the mucoid strains do not lose the QS regulation or the ability to produce rhamnolipids until the late stage of the chronic infection.

AB - Pseudomonas aeruginosa is the predominant microorganism in chronic lung infection of cystic fibrosis patients. The chronic lung infection is preceded by intermittent colonization. When the chronic infection becomes established, it is well accepted that the isolated strains differ phenotypically from the intermittent strains. Dominating changes are the switch to mucoidity (alginate overproduction) and loss of epigenetic regulation of virulence such as the Quorum Sensing (QS). To elucidate the dynamics of P. aeruginosa QS systems during long term infection of the CF lung, we have investigated 238 isolates obtained from 152 CF patients at different stages of infection ranging from intermittent to late chronic. Isolates were characterized with regard to QS signal molecules, alginate, rhamnolipid and elastase production and mutant frequency. The genetic basis for change in QS regulation were investigated and identified by sequence analysis of lasR, rhlR, lasI and rhlI. The first QS system to be lost was the one encoded by las system 12 years (median value) after the onset of the lung infection with subsequent loss of the rhl encoded system after 17 years (median value) shown as deficiencies in production of the 3-oxo-C12-HSL and C4-HSL QS signal molecules respectively. The concomitant development of QS malfunction significantly correlated with the reduced production of rhamnolipids and elastase and with the occurrence of mutations in the regulatory genes lasR and rhlR. Accumulation of mutations in both lasR and rhlR correlated with development of hypermutability. Interestingly, a higher number of mucoid isolates were found to produce C4-HSL signal molecules and rhamnolipids compared to the non-mucoid isolates. As seen from the present data, we can conclude that P. aeruginosa and particularly the mucoid strains do not lose the QS regulation or the ability to produce rhamnolipids until the late stage of the chronic infection.

U2 - 10.1371/journal.pone.0010115

DO - 10.1371/journal.pone.0010115

M3 - Journal article

C2 - 20404933

VL - 5

SP - e10115

JO - PLoS ONE

JF - PLoS ONE

SN - 1932-6203

IS - 4

ER -

ID: 20393037