Pseudomonas aeruginosa Biofilms in the Lungs of Cystic Fibrosis Patients

Niels Høiby; Helle Krogh Johansen; Claus Moser; Oana Ciofu; Peter Østrup Jensen; Mette Kolpen; Lotte Mandsberg; Michael Givskov; Søren Molin; Thomas Bjarnsholt

doi:10.1007/978-1-4419-6084-9_10

Pseudomonas aeruginosa Biofilms in the Lungs of Cystic Fibrosis Patients

Niels Høiby^*, Helle Krogh Johansen, Claus Moser, Oana Ciofu, Peter Østrup Jensen, Mette Kolpen, Lotte Mandsberg, Michael Givskov, Søren Molin, Thomas Bjarnsholt

^*Corresponding author for this work

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

3 Citations (Scopus)

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.

Original language	English
Title of host publication	Biofilm Infections
Number of pages	18
Publisher	Springer
Publication date	2011
Pages	167-184
ISBN (Print)	9781441960832
DOIs	https://doi.org/10.1007/978-1-4419-6084-9_10
Publication status	Published - 2011

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

Cite this

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

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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.",

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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

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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.

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