Gelsolin, but not mucin, inhibits P. aeruginosa swimming motility in vitro

Pseudomonas aeruginosa is a ubiquitous, opportunistic pathogen responsible for substantial morbidity and mortality in patients with cystic fibrosis (CF). Following initial colonization of the CF lung, P. aeruginosa changes phenotype and becomes virtually impossible to inhibit, kill, or remove. Thus, understanding and preventing initial P. aeruginosa colonization is of great interest. Our lab has previously demonstrated that apical secretions from a human airway cell line, Calu‐3, inhibit P. aeruginosa swimming motility and biofilm formation in vitro, and that this inhibition is lost if proteins > 50 kDa are removed. However, secretions from Calu‐3 cells lacking the CFTR (CF‐like cells) do not inhibit P. aeruginosa . The goal of this project is to identify the inhibitory protein(s) present in non‐CF apical airway secretions. Using reducing SDS‐PAGE, we identified a band at approximately 90 – 100 kDa that was present in normal apical airway secretions but not CF‐like secretions, suggesting that a protein this size may be our target. We have begun testing readily available candidate proteins – mucin and gelsolin ‐‐ to see if they can replicate the inhibitory activity of non‐CF airway secretions. Mucin had no effect on P. aeruginosa swimming motility or biofilm formation, but gelsolin significantly inhibited swimming motility in a dose‐dependent manner. Interestingly, P. aeruginosa biofilm formation was not inhibited by gelsolin. Thus, gelsolin may be responsible for at least a part of the P. aeruginosa inhibition induced by apical airway secretions. Support or Funding Information Funding provided by Augsburg College Undergraduate Research and Graduate Opportunities Office and the Augsburg College Biology Department