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Pseudomonas aeruginosa-Human Airway Epithelial Cell Interaction*: Effects of Iron on Inflammation and Apoptosis

Milene Saavedra, MD; Michael Vasil, PhD; Scott Randell, PhD; James West, PhD, MD; David Rodman, MD
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*From the Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, CO.

Correspondence to: Milene Saavedra, MD, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, 4200 E. 9th Ave, Box C272, Denver, CO 80262; e-mail: Saavedra@UCHSC.edu



Chest. 2002;121(3_suppl):40S-42S. doi:10.1378/chest.121.3_suppl.40S
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A unique host pathogen relationship exists between Pseudomonas aeruginosa and human airway epithelium (HAE) in patients with cystic fibrosis. Chronic colonization of P aeruginosa in cystic fibrosis airways is a major source of morbidity and mortality in these patients. Iron (Fe) availability regulates the virulence of P aeruginosa, but the effect of altered Fe availability on the host-pathogen relationship is not known. P aeruginosa is an obligate respirer, utilizing oxygen or nitrate. It cannot perform its respiratory functions without Fe. This need for Fe also places the bacterium at a high potential for Fe-catalyzed oxidative stress. P aeruginosa specifically requires reduced Fe2+, a soluble form of Fe. In the microenvironments of lungs and blood, high oxygen concentrations lead to formation of the oxidized insoluble form of Fe, specifically Fe3+. Fe is further made inaccessible by binding to transferrin and lactoferrin. P aeruginosa requires Fe2+ concentrations of 10-6 M to survive, whereas it encounters environmental concentrations of 10-18 M. The pursuit of Fe is mediated through various mechanisms including: (1) production of proteases to degrade host Fe binding compounds; (2) release of Fe binding compounds, siderophores, which bind the free Fe3+ released from host lactoferrin and transferrin following exposure to proteases; (3) reduction of insoluble Fe3+ to soluble Fe2+ by membrane reductases; and (4) production of compounds such as exotoxins that are toxic to eukaryotic cells, eliminating competition for usable Fe.1

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