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Human Airway Secretions Inhibit Pseudomonas aeruginosa Activity: Effects on Survival, Growth, and Flagellar Motility
Author(s) -
Weitz Anna K,
Willborg Jessica L,
Hinz Sandra M,
BankersFulbright Jennifer L
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.131.10
Subject(s) - pseudomonas aeruginosa , microbiology and biotechnology , motility , colonization , cystic fibrosis , virulence , secretion , biofilm , biology , airway , epithelium , pathogen , bacteria , medicine , endocrinology , biochemistry , gene , genetics , surgery
Pseudomonas aeruginosa is a ubiquitous opportunistic pathogen that is a leading cause of morbidity and mortality in patients with cystic fibrosis (CF). The relative selectivity of P. aeruginosa colonization in CF patients suggests that the CF airway, in contrast to normal airways, is particularly hospitable to P. aeruginosa . One likely possibility for this difference is that normal but not CF airways secrete compounds that attenuate the virulence of P. aeruginosa and prevent colonization. In this study, we examined the ability of normal airway epithelial secretions to inhibit two properties of P. aeruginosa associated with colonization: proliferation and flagellar motility. For these initial experiments, we used apical secretions from polarized Calu‐3 cell monolayers and the P. aeruginosa strain PA14. Treatment of PA14 cells with Calu‐3 secretions dramatically reduced both average swimming speed (30 vs. 15 μm/sec) and the number of motile bacteria (56% vs. 42%). Inhibition of PA14 growth was not seen after 24‐hours of incubation with Calu‐3 secretions, in contrast to previous reports. Our preliminary attempts to identify the active component(s) in Calu‐3 secretions suggest that one or more proteins >;50 kDa are responsible. We conclude that normal airway epithelial secretions directly inhibit certain P. aeruginosa functions associated with airway colonization. This project was funded by the Augsburg College Undergraduate Research and Graduate Opportunities (URGO) Office and Sundquist Scholars Program.