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The ΔF508-CFTR mutation results in increased biofilm formation by Pseodomonas aeruginosa by increasing iron availability

Moreau-Marquis, Sophie, Bomberger, Jennifer M., Anderson, Gregory G., Swiatecka-Urban, Agnieszka, Ye, Siying, O'Toole, George A. and Stanton, Bruce A. 2008, The ΔF508-CFTR mutation results in increased biofilm formation by Pseodomonas aeruginosa by increasing iron availability, American journal of physiology : lung cellular and molecular physiology, vol. 295, no. 1, pp. 25-37, doi: 10.1152/ajplung.00391.2007.

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Title The ΔF508-CFTR mutation results in increased biofilm formation by Pseodomonas aeruginosa by increasing iron availability
Author(s) Moreau-Marquis, Sophie
Bomberger, Jennifer M.
Anderson, Gregory G.
Swiatecka-Urban, Agnieszka
Ye, Siying
O'Toole, George A.
Stanton, Bruce A.
Journal name American journal of physiology : lung cellular and molecular physiology
Volume number 295
Issue number 1
Start page 25
End page 37
Total pages 13
Publisher American Physiological Society
Place of publication Bethesda, Md.
Publication date 2008-07
ISSN 1040-0605
Keyword(s) cystic fibrosis transmembrane conductance regulator
airway
Summary Enhanced antibiotic resistance of Pseudomonas aeruginosa in the cystic fibrosis (CF) lung is thought to be due to the formation of biofilms. However, there is no information on the antibiotic resistance of P. aeruginosa biofilms grown on human airway epithelial cells or on the effects of airway cells on biofilm formation by P. aeruginosa. Thus we developed a coculture model and report that airway cells increase the resistance of P. aeruginosa to tobramycin (Tb) by >25-fold compared with P. aeruginosa grown on abiotic surfaces. Therefore, the concentration of Tb required to kill P. aeruginosa biofilms on airway cells is 10-fold higher than the concentration achievable in the lungs of CF patients. In addition, CF airway cells expressing ΔF508-CFTR significantly enhanced P. aeruginosa biofilm formation, and ΔF508 rescue with wild-type CFTR reduced biofilm formation. Iron (Fe) content of the airway in CF is elevated, and Fe is known to enhance P. aeruginosa growth. Thus we investigated whether enhanced biofilm formation on ΔF508-CFTR cells was due to increased Fe release by airway cells. We found that airway cells expressing ΔF508-CFTR released more Fe than cells rescued with WT-CFTR. Moreover, Fe chelation reduced biofilm formation on airway cells, whereas Fe supplementation enhanced biofilm formation on airway cells expressing WT-CFTR. These data demonstrate that human airway epithelial cells promote the formation of P. aeruginosa biofilms with a dramatically increased antibiotic resistance. The ΔF508-CFTR mutation enhances biofilm formation, in part, by increasing Fe release into the apical medium.
Language eng
DOI 10.1152/ajplung.00391.2007
Field of Research 119999 Medical and Health Sciences not elsewhere classified
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2008, American Physiological Society
Persistent URL http://hdl.handle.net/10536/DRO/DU:30040953

Document type: Journal Article
Collection: School of Medicine
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