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Functional Effects of Nanoparticle Exposure on Calu-3 Airway Epithelial CellsBanga A.1 · Witzmann F.A.2 · Petrache H.I.3 · Blazer-Yost B.L.1,2
1Department of Biology, Indiana University Purdue University Indianapolis,2Department of Cellular & Integrative Physiology, Indiana University School of Medicine Indianapolis,3Department of Physics, Indiana University Purdue University Indianapolis Corresponding Author
Bonnie L. Blazer-Yost
Indiana University - Purdue University
Biology Department, SL 358 - 723 West Michigan Street
Indianapolis, IN 46202 (USA)
Tel. +1 317-278-1145, Fax +1 317-274-2846, E-Mail email@example.com
High concentrations of manufactured carbon nanoparticles (CNP) are known to cause oxidative stress, inflammatory responses and granuloma formation in respiratory epithelia. To examine the effects of lower, more physiologically relevant concentrations, the human airway epithelial cell line, Calu-3, was used to evaluate potential alterations in transepithelial permeability and cellular function of airway epithelia after exposure to environmentally realistic concentrations of carbon nanoparticles. Three common carbon nanoparticles, fullerenes, single- and multi-wall carbon nanotubes (SWCNT, MWCNT) were used in these experiments. Electrophysiological measurements were performed to assay transepithelial electrical resistance (TEER) and epinephrine-stimulated chloride (Cl-) ion secretion of epithelial cell monolayers that had been exposed to nanoparticles for three different times (1 h, 24 h and 48 h) and over a 7 log unit range of concentrations. Fullerenes did not have any effect on the TEER or stimulated ion transport. However, the carbon nanotubes (CNT) significantly decreased TEER and inhibited epinephrine-stimulated Cl- secretion. The changes were time dependent and at more chronic exposures caused functional effects which were evident at concentrations substantially lower than have been previously examined. The functional changes manifested in response to physiologically relevant exposures would inhibit mucociliary clearance mechanisms and compromise the barrier function of airway epithelia.
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