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Faculty Mentor

Jennifer L. Bankers-Fulbright, Ph.D.


Cystic fibrosis (CF) is a genetic disease caused by the mutation of the cystic fibrosis transmembrane regulator (CFTR) protein, which normally transports anions across cell membranes. Dysfunction of the CFTR on airway epithelial cells reduces the levels and/or activity of several antimicrobial molecules secreted by these cells, and may contribute to the persistence of bacteria such as Staphylococcus aureus and Pseudomonas aeruginosa in the lungs of patients with CF. Thus, we hypothesize that normal human airway epithelial cells secrete one or more active molecules that inhibit functions related to S. aureus and P. aeruginosa growth and/or biofilm formation. To test this hypothesis, we quantified the effects of apical airway epithelial cell secretions on the growth rate and static biofilm formation of S. aureus and P. aeruginosa. The apical secretions dose-dependently inhibited S. aureus biofilm formation but had no effect on the rate of S. aureus growth. Conversely, P. aeruginosa biofilm formation was not affected by the apical secretions, but its growth rate was dose-dependently inhibited. Boiling the apical secretions for 10 minutes at 100 °C resulted in increased inhibition of S. aureus biofilm formation, and reversed the inhibition of P. aeruginosa growth. This suggests that there may be more than one molecule involved with these inhibitory effects.

Publication Date



cystic fibrosis, epithelial secretions, bacterial infection


Cell Biology

Human Airway Epithelial Secretions Differentially Inhibit Staphylococcus aureus and Pseudomonas aeruginosa Functions