Coal fly ash impairs airway antimicrobial peptides and increases bacterial growth.

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TitleCoal fly ash impairs airway antimicrobial peptides and increases bacterial growth.
Publication TypeJournal Article
Year of Publication2013
JournalPLoS One
Volume8
Issue2
Paginatione57673
AuthorsBorcherding, Jennifer A., Haihan Chen, Juan C. Caraballo, Jonas Baltrusaitis, Alejandro A. Pezzulo, Joseph Zabner, Vicki H. Grassian, and Alejandro P. Comellas
PublisherPublic Library of Science
ISBN Number1932-6203
Abstract

Air pollution is a risk factor for respiratory infections, and one of its main components is particulate matter (PM), which is comprised of a no. of particles that contain iron, such as coal fly ash (CFA). Since free iron concns. are extremely low in airway surface liq. (ASL), we hypothesize that CFA impairs antimicrobial peptides (AMP) function and can be a source of iron to bacteria. We tested this hypothesis in vivo by instilling mice with Pseudomonas aeruginosa (PA01) and CFA and det. the percentage of bacterial clearance. In addn., we tested bacterial clearance in cell culture by exposing primary human airway epithelial cells to PA01 and CFA and detg. the AMP activity and bacterial growth in vitro. We report that CFA is a bioavailable source of iron for bacteria. We show that CFA interferes with bacterial clearance in vivo and in primary human airway epithelial cultures. Also, we demonstrate that CFA inhibits AMP activity in vitro, which we propose as a mechanism of our cell culture and in vivo results. Furthermore, PA01 uses CFA as an iron source with a direct correlation between CFA iron dissoln. and bacterial growth. CFA concns. used are very relevant to human daily exposures, thus posing a potential public health risk for susceptible subjects. Although CFA provides a source of bioavailable iron for bacteria, not all CFA particles have the same biol. effects, and their propensity for iron dissoln. is an important factor. CFA impairs lung innate immune mechanisms of bacterial clearance, specifically AMP activity. We expect that identifying the PM mechanisms of respiratory infections will translate into public health policies aimed at controlling, not only concn. of PM exposure, but physicochem. characteristics that will potentially cause respiratory infections in susceptible individuals and populations. [on SciFinder(R)]