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Human Airway Epithelial Secretions Inhibit the Formation of Pseudomonas aeruginosa Biofilms
Author(s) -
Sorum Alexander W,
Zank Allison 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.645.8
Subject(s) - pseudomonas aeruginosa , biofilm , microbiology and biotechnology , cystic fibrosis , secretion , epithelium , pathogen , in vivo , biology , bacteria , respiratory epithelium , colonization , airway , chemistry , medicine , biochemistry , surgery , genetics
Pseudomonas aeruginosa is a ubiquitous opportunistic pathogen that rarely causes respiratory disease except in individuals with specific risk factors, such as cystic fibrosis (CF). The ability of P. aeruginosa to readily form biofilms in vivo is associated with airway colonization in susceptible individuals. Thus, we hypothesized that non‐CF airway epithelial cells secrete one or more compounds that inhibit P. aeruginosa biofilm formation. To test this, we modified and optimized a static biofilm assay and tested the ability of apical Calu‐3 cell secretions to inhibit biofilm formation by the P. aeruginosa strain, PA14. PA14 formed robust biofilms after 18–24 hours, and biofilm formation was significantly inhibited in the presence of Calu‐3 secretions. Preliminary experiments using secretions from a Calu‐3 cell line not expressing the CF transmembrane regulator (CFTR) suggest that CF‐like secretions do not inhibit PA14 biofilm formation. Thus, normal airway epithelial cells, but not CF‐like epithelial cells, appear to secrete one or more compounds that inhibit P. aeruginosa biofilm formation. This project was funded by the Augsburg College Undergraduate Research and Graduate Opportunities (URGO) Office, the Augsburg Sundquist Scholars Program, the Augsburg McNair Scholars Program, and the Augsburg Department of Biology.