The role of the CFTR in susceptibility to Pseudomonas aeruginosa infections in  cystic fibrosis.
Recent molecular and cellular studies have shed new light on the basis for the susceptibility of cystic fibrosis (CF) patients to Pseudomonas aeruginosa infection. Changes in airway liquid composition and/or viscosity, enhanced bacterial binding to mucin and epithelial cell receptors, increased innate inflammation owing to disruptions in lipid metabolism and a role for the CFTR protein in bacterial ingestion and clearance have all been postulated. The high P. aeruginosa infection rate in CF patients can potentially be explained by the specificity of the interaction between the CFTR and P. aeruginosa.
Goldberg
J B
JB
Dept of Microbiology, University of Virginia Health Science Center, Charlottesville 22908, USA.
Pier
G B
GB
D000818:Animals; D003550:Cystic Fibrosis / Q000150:complications* / Q000235:genetics / Q000378:metabolism / Q000382:microbiology; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000235:genetics / Q000378:metabolism*; D004198:Disease Susceptibility; D006801:Humans; D051379:Mice; D009154:Mutation; D011552:Pseudomonas Infections / Q000209:etiology* / Q000382:microbiology; D011550:Pseudomonas aeruginosa / Q000378:metabolism / Q000472:pathogenicity*
C505032:CFTR protein, human; D019005:Cystic Fibrosis Transmembrane Conductance Regulator