Pseudomonas aeruginosa biofilms in cystic fibrosis

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Pseudomonas aeruginosa biofilms in cystic fibrosis. / Høiby, Niels; Ciofu, Oana; Bjarnsholt, Thomas.

In: Future Microbiology, Vol. 5, 01.11.2010, p. 1663-74.

Research output: Contribution to journalReviewpeer-review

Harvard

Høiby, N, Ciofu, O & Bjarnsholt, T 2010, 'Pseudomonas aeruginosa biofilms in cystic fibrosis', Future Microbiology, vol. 5, pp. 1663-74. https://doi.org/10.2217/fmb.10.125, https://doi.org/10.2217/fmb.10.125

APA

Høiby, N., Ciofu, O., & Bjarnsholt, T. (2010). Pseudomonas aeruginosa biofilms in cystic fibrosis. Future Microbiology, 5, 1663-74. https://doi.org/10.2217/fmb.10.125, https://doi.org/10.2217/fmb.10.125

Vancouver

Høiby N, Ciofu O, Bjarnsholt T. Pseudomonas aeruginosa biofilms in cystic fibrosis. Future Microbiology. 2010 Nov 1;5:1663-74. https://doi.org/10.2217/fmb.10.125, https://doi.org/10.2217/fmb.10.125

Author

Høiby, Niels ; Ciofu, Oana ; Bjarnsholt, Thomas. / Pseudomonas aeruginosa biofilms in cystic fibrosis. In: Future Microbiology. 2010 ; Vol. 5. pp. 1663-74.

Bibtex

@article{558d999497da4613aca54e96e33f6c66,
title = "Pseudomonas aeruginosa biofilms in cystic fibrosis",
abstract = "The persistence of chronic Pseudomonas aeruginosa lung infections in cystic fibrosis (CF) patients is due to biofilm-growing mucoid (alginate-producing) strains. A biofilm is a structured consortium of bacteria, embedded in a self-produced polymer matrix consisting of polysaccharide, protein and DNA. In CF lungs, the polysaccharide alginate is the major part of the P. aeruginosa biofilm matrix. Bacterial biofilms cause chronic infections because they show increased tolerance to antibiotics and resist phagocytosis, as well as other components of the innate and the adaptive immune system. As a consequence, a pronounced antibody response develops, leading to immune complex-mediated chronic inflammation, dominated by polymorphonuclear leukocytes. The chronic inflammation is the major cause of the lung tissue damage in CF. Biofilm growth in CF lungs is associated with an increased frequency of mutations, slow growth and adaptation of the bacteria to the conditions in the lungs, and to antibiotic therapy. Low bacterial metabolic activity and increase of doubling times of the bacterial cells in CF lungs are responsible for some of the tolerance to antibiotics. Conventional resistance mechanisms, such as chromosomal {\ss}-lactamase, upregulated efflux pumps, and mutations of antibiotic target molecules in the bacteria, also contribute to the survival of P. aeruginosa biofilms. Biofilms can be prevented by early aggressive antibiotic prophylaxis or therapy, and they can be treated by chronic suppressive therapy.",
author = "Niels H{\o}iby and Oana Ciofu and Thomas Bjarnsholt",
year = "2010",
month = nov,
day = "1",
doi = "10.2217/fmb.10.125",
language = "English",
volume = "5",
pages = "1663--74",
journal = "Future Microbiology",
issn = "1746-0913",
publisher = "Future Medicine Ltd.",

}

RIS

TY - JOUR

T1 - Pseudomonas aeruginosa biofilms in cystic fibrosis

AU - Høiby, Niels

AU - Ciofu, Oana

AU - Bjarnsholt, Thomas

PY - 2010/11/1

Y1 - 2010/11/1

N2 - The persistence of chronic Pseudomonas aeruginosa lung infections in cystic fibrosis (CF) patients is due to biofilm-growing mucoid (alginate-producing) strains. A biofilm is a structured consortium of bacteria, embedded in a self-produced polymer matrix consisting of polysaccharide, protein and DNA. In CF lungs, the polysaccharide alginate is the major part of the P. aeruginosa biofilm matrix. Bacterial biofilms cause chronic infections because they show increased tolerance to antibiotics and resist phagocytosis, as well as other components of the innate and the adaptive immune system. As a consequence, a pronounced antibody response develops, leading to immune complex-mediated chronic inflammation, dominated by polymorphonuclear leukocytes. The chronic inflammation is the major cause of the lung tissue damage in CF. Biofilm growth in CF lungs is associated with an increased frequency of mutations, slow growth and adaptation of the bacteria to the conditions in the lungs, and to antibiotic therapy. Low bacterial metabolic activity and increase of doubling times of the bacterial cells in CF lungs are responsible for some of the tolerance to antibiotics. Conventional resistance mechanisms, such as chromosomal ß-lactamase, upregulated efflux pumps, and mutations of antibiotic target molecules in the bacteria, also contribute to the survival of P. aeruginosa biofilms. Biofilms can be prevented by early aggressive antibiotic prophylaxis or therapy, and they can be treated by chronic suppressive therapy.

AB - The persistence of chronic Pseudomonas aeruginosa lung infections in cystic fibrosis (CF) patients is due to biofilm-growing mucoid (alginate-producing) strains. A biofilm is a structured consortium of bacteria, embedded in a self-produced polymer matrix consisting of polysaccharide, protein and DNA. In CF lungs, the polysaccharide alginate is the major part of the P. aeruginosa biofilm matrix. Bacterial biofilms cause chronic infections because they show increased tolerance to antibiotics and resist phagocytosis, as well as other components of the innate and the adaptive immune system. As a consequence, a pronounced antibody response develops, leading to immune complex-mediated chronic inflammation, dominated by polymorphonuclear leukocytes. The chronic inflammation is the major cause of the lung tissue damage in CF. Biofilm growth in CF lungs is associated with an increased frequency of mutations, slow growth and adaptation of the bacteria to the conditions in the lungs, and to antibiotic therapy. Low bacterial metabolic activity and increase of doubling times of the bacterial cells in CF lungs are responsible for some of the tolerance to antibiotics. Conventional resistance mechanisms, such as chromosomal ß-lactamase, upregulated efflux pumps, and mutations of antibiotic target molecules in the bacteria, also contribute to the survival of P. aeruginosa biofilms. Biofilms can be prevented by early aggressive antibiotic prophylaxis or therapy, and they can be treated by chronic suppressive therapy.

U2 - 10.2217/fmb.10.125

DO - 10.2217/fmb.10.125

M3 - Review

C2 - 21133688

VL - 5

SP - 1663

EP - 1674

JO - Future Microbiology

JF - Future Microbiology

SN - 1746-0913

ER -

ID: 32244198