Pseudomonas aeruginosa Biofilms in the Lungs of Cystic Fibrosis Patients

Research output: Chapter in Book/Report/Conference proceeding › Book chapter › Research › peer-review

Standard

Pseudomonas aeruginosa Biofilms in the Lungs of Cystic Fibrosis Patients. / Høiby, Niels; Johansen, Helle Krogh; Moser, Claus; Ciofu, Oana; Jensen, Peter Østrup; Kolpen, Mette; Mandsberg, Lotte; Givskov, Michael; Molin, Søren; Bjarnsholt, Thomas.

Biofilm Infections. Springer, 2011. p. 167-184.

Research output: Chapter in Book/Report/Conference proceeding › Book chapter › Research › peer-review

Harvard

Høiby, N, Johansen, HK, Moser, C, Ciofu, O, Jensen, PØ, Kolpen, M, Mandsberg, L, Givskov, M, Molin, S & Bjarnsholt, T 2011, Pseudomonas aeruginosa Biofilms in the Lungs of Cystic Fibrosis Patients. in Biofilm Infections. Springer, pp. 167-184. https://doi.org/10.1007/978-1-4419-6084-9_10

APA

Høiby, N., Johansen, H. K., Moser, C., Ciofu, O., Jensen, P. Ø., Kolpen, M., Mandsberg, L., Givskov, M., Molin, S., & Bjarnsholt, T. (2011). Pseudomonas aeruginosa Biofilms in the Lungs of Cystic Fibrosis Patients. In Biofilm Infections (pp. 167-184). Springer. https://doi.org/10.1007/978-1-4419-6084-9_10

Vancouver

Høiby N, Johansen HK, Moser C, Ciofu O, Jensen PØ, Kolpen M et al. Pseudomonas aeruginosa Biofilms in the Lungs of Cystic Fibrosis Patients. In Biofilm Infections. Springer. 2011. p. 167-184 https://doi.org/10.1007/978-1-4419-6084-9_10

Author

Høiby, Niels ; Johansen, Helle Krogh ; Moser, Claus ; Ciofu, Oana ; Jensen, Peter Østrup ; Kolpen, Mette ; Mandsberg, Lotte ; Givskov, Michael ; Molin, Søren ; Bjarnsholt, Thomas. / Pseudomonas aeruginosa Biofilms in the Lungs of Cystic Fibrosis Patients. Biofilm Infections. Springer, 2011. pp. 167-184

Bibtex

@inbook{dd4676f10bc64b1ab3f2139c3d23964d,
title = "Pseudomonas aeruginosa Biofilms in the Lungs of Cystic Fibrosis Patients",
abstract = "The consequence of the mutations in the CFTR gene is malfunction of the chloride channel in cystic fibrosis (CF) patients, which leads to decreased volume of the paraciliary fluid in the lower respiratory tract, and that in turn leads to impaired mucociliary clearance of inhaled microbes (Boucher 2004). This impairment of the non-inflammatory defense mechanism of the respiratory tract leads to early recruitment of the inflammatory defense mechanisms, e.g., polymorphonuclear leukocytes (PMN) and antibodies (Armstrong et al. 1995, 2005, Hoiby et al. 2001). CF patients, therefore, from early childhood suffer from recurrent and chronic respiratory tract infections characterized by PMN inflammation.",
author = "Niels H{\o}iby and Johansen, {Helle Krogh} and Claus Moser and Oana Ciofu and Jensen, {Peter {\O}strup} and Mette Kolpen and Lotte Mandsberg and Michael Givskov and S{\o}ren Molin and Thomas Bjarnsholt",
year = "2011",
doi = "10.1007/978-1-4419-6084-9_10",
language = "English",
isbn = "9781441960832",
pages = "167--184",
booktitle = "Biofilm Infections",
publisher = "Springer",
address = "Switzerland",

}

RIS

TY - CHAP

T1 - Pseudomonas aeruginosa Biofilms in the Lungs of Cystic Fibrosis Patients

AU - Høiby, Niels

AU - Johansen, Helle Krogh

AU - Moser, Claus

AU - Ciofu, Oana

AU - Jensen, Peter Østrup

AU - Kolpen, Mette

AU - Mandsberg, Lotte

AU - Givskov, Michael

AU - Molin, Søren

AU - Bjarnsholt, Thomas

PY - 2011

Y1 - 2011

N2 - The consequence of the mutations in the CFTR gene is malfunction of the chloride channel in cystic fibrosis (CF) patients, which leads to decreased volume of the paraciliary fluid in the lower respiratory tract, and that in turn leads to impaired mucociliary clearance of inhaled microbes (Boucher 2004). This impairment of the non-inflammatory defense mechanism of the respiratory tract leads to early recruitment of the inflammatory defense mechanisms, e.g., polymorphonuclear leukocytes (PMN) and antibodies (Armstrong et al. 1995, 2005, Hoiby et al. 2001). CF patients, therefore, from early childhood suffer from recurrent and chronic respiratory tract infections characterized by PMN inflammation.

AB - The consequence of the mutations in the CFTR gene is malfunction of the chloride channel in cystic fibrosis (CF) patients, which leads to decreased volume of the paraciliary fluid in the lower respiratory tract, and that in turn leads to impaired mucociliary clearance of inhaled microbes (Boucher 2004). This impairment of the non-inflammatory defense mechanism of the respiratory tract leads to early recruitment of the inflammatory defense mechanisms, e.g., polymorphonuclear leukocytes (PMN) and antibodies (Armstrong et al. 1995, 2005, Hoiby et al. 2001). CF patients, therefore, from early childhood suffer from recurrent and chronic respiratory tract infections characterized by PMN inflammation.

U2 - 10.1007/978-1-4419-6084-9_10

DO - 10.1007/978-1-4419-6084-9_10

M3 - Book chapter

AN - SCOPUS:84900759179

SN - 9781441960832

SP - 167

EP - 184

BT - Biofilm Infections

PB - Springer

ER -

ID: 340023855