help button home button
AJRCMB
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Published ahead of print on March 8, 2007, doi:10.1165/rcmb.2006-0419OC

Am. J. Respir. Cell Mol. Biol., Volume 37, Number 1, July 2007, 97-104

A more recent version of this article appeared on July 1, 2007
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
2006-0419OCv1
37/1/97    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Suresh, V.
Right arrow Articles by George, S. C
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Suresh, V.
Right arrow Articles by George, S. C

Submitted on November 8, 2006
Revised on March 7, 2007

Measurement of IL-13-induced iNOS-derived Gas Phase Nitric Oxide in Human Bronchial Epithelial Cells

Vinod Suresh1, Justin D Mih1, and Steven C George2*

1 Department of Biomedical Engineering, University of California, Irvine, Irvine, CA, USA, 2 Department of Biomedical Engineering, University of California, Irvine, Irvine, CA, USA; Department of Chemical Engineering and Materials Science, University of California, Irvine, Irvine, CA, USA

* To whom correspondence should be addressed. E-mail: scgeorge{at}uci.edu.

Exhaled nitric oxide (NO) is altered in numerous diseases including asthma, and is thought broadly to be a non-invasive marker of inflammation. However, the precise source of exhaled nitric oxide has yet to be identified, and the interpretation is further hampered by significant inter-subject variation. Using fully differentiated normal human bronchial epithelial (NHBE) cells we sought to determine 1) the rate of NO release (flux, pl.s-1.cm-2) into the gas, 2) the effect of interleukin (IL)-13, a prominent mediator of allergic inflammation, on NO release, and 3) inter-subject/donor variability in NO release. NHBE cells from three different donors were cultured at an air-liquid interface and stimulated with different concentrations of IL-13 (0, 1 and 10 ng/mL) for 48 hours. Gas phase NO concentrations in the headspace over the cells were measured using a chemiluminescence analyzer. The basal NO flux from the three donors (0.05 ± 0.03) is similar in magnitude to that estimated from exhaled NO concentrations, and was significantly increased by IL-13 in a donor specific fashion. The increase in NO release was strongly correlated with inducible nitric oxide synthase (iNOS) gene and protein expression. There was a trend toward enhanced production of nitrate relative to nitrite as an end product of NO metabolism in IL-13 stimulated cells. NO release from airway epithelial cells can be directly measured. The rate of release in response to IL-13 is strongly dependent on the individual donor, but is primarily due to the expression of iNOS.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Proc. Am. Thorac. Soc. Am. J. Respir. Crit. Care Med.
Copyright © 2007 American Thoracic Society. 		  2009/2010 ATS Fellows Career Development Awards