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Pseudomonas aeruginosa  establishes airway infections in Cystic Fibrosis patients. Here, we investigate the molecular interactions between  P. aeruginosa  and airway mucus secretions (AMS) derived from the primary cultures of normal human tracheal epithelial (NHTE) cells. PAO1, a prototype strain of  P. aeruginosa , was capable of proliferating during incubation with AMS, while all other tested bacterial species perished. A PAO1 mutant lacking  PA4834  gene became susceptible to AMS treatment. The Δ PA4834  mutant was grown in AMS supplemented with 100 μM ferric iron, suggesting that the  PA4834  gene product is involved in iron metabolism. Consistently, intracellular iron content was decreased in the mutant, but not in PAO1 after the AMS treatment. Importantly, a PAO1 mutant unable to produce both pyoverdine and pyochelin remained viable, suggesting that these two major siderophore molecules are dispensable for maintaining viability during incubation with AMS. The Δ PA4834  mutant was regrown in AMS amended with 100 μM nicotianamine, a phytosiderophore whose production is predicted to be mediated by the  PA4836  gene. Infectivity of the Δ PA4834  mutant was also significantly compromised  in vivo . Together, our results identify a genetic element encoding a novel iron acquisition system that plays a previously undiscovered role in  P. aeruginosa  airway infection.

A novel siderophore system is essential for the growth of Pseudomonas aeruginosa in airway mucus