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HERO ID
2625451
Reference Type
Journal Article
Subtype
Abstract
Title
Particulate matter alters airway epithelial barrier function
Author(s)
Sidhaye, V; Chau, E; Breysse, P; King, LS
Year
2010
Is Peer Reviewed?
Yes
Journal
American Journal of Respiratory and Critical Care Medicine
ISSN:
1073-449X
EISSN:
1535-4970
Volume
181
Page Numbers
A6392
Language
English
DOI
10.1164/ajrccm-conference.2010.181.1_MeetingAbstracts.A6392
Web of Science Id
WOS:000208771005011
Relationship(s)
is part of a larger document
3452678
Proceedings of the American Thoracic Society 2010 International Conference, May 14-19, 2010, New Orleans
Abstract
Rationale: The airway epithelia are exposed to both biophysical and chemical stimuli from the lumen of the airway, some of which are physiologic such as airflow-induced shear stress, and others that are pathologic such as particulate matter (PM). We have previously shown that in both cell culture and in mice trachea that low levels of shear stress caused by tidal volume breathing enhances epithelial barrier function (decreased permeability of evans blue dye-4% albumin or FITC-dextran) in part by reducing the abundance of AQP5, an apical water channel. The effects of a pathologic stimulus such as particulate matter on airway epithelial barrier function are unknown, despite the airway epithelial cells being the first line of exposure to inhaled particulate matter.
Method: Primary airway epithelial cells grown on an air-liquid interface were exposed to different doses of PM(collected from a high-volume cyclone collector) for varying durations and cell responses were assessed by changes in permeability (FITC-dextran), protein abundance and localization.
Results: A single treatment with PM (50-150ug/ml) leads to enhancement of barrier, and a decrease in AQP5 abundance. This reduction in AQP5 results in microtubule destabilization, which our data suggests leads to enhanced barrier function in airway epithelial cells. However, repeated exposure to particulate matter results in barrier disruption despite slight further reductions in AQP5.
Conclusion: In contrast to data published on endothelial cells, we observed that in response to an initial exposure to PM, the airway epithelial barrier is enhanced in association with cytoskeletal modifications. However, airway epithelial cells are unable to further accommodate in response to repetitive insults, leading to barrier dysfunction.
Conference Name
American Thoracic Society 2010 International Conference
Conference Location
New Orleans, LA
Conference Dates
May 14-19, 2010
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