HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:
Guest Access | Sign In via User Name/Password

This Article Full Text Free Full Text (PDF) Free Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Add to My Personal Article Archive Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Hussain, I. Articles by Kline, J. Search for Related Content PubMed PubMed Citation Articles by Hussain, I. Articles by Kline, J.

Effect of Nitrogen Dioxide Exposure on Allergic Asthma in a Murine Model^*

^* From the Department of Medicine (Dr. Hussain), Washington University School of Medicine, St. Louis, MO; the Division of Pulmonary Medicine (Mr. Businga and Dr. Kline), Department of Internal Medicine, Roy J. and Lucille A. Carver College of Medicine, and the Department of Occupational and Environmental Medicine (Dr. O’Shaughnessy), College of Public Health, University of Iowa, Iowa City, IA; and the Department of Medicine (Dr. Jain), University of California San Francisco-Fresno, Fresno, CA.

Correspondence to: Joel Kline, MD, FCCP, C33 GH, UIHC, 200 Hawkins Dr, Iowa City, IA 52242; e-mail: joel-kline{at}uiowa.edu

Study objectives: The purpose of this study was to examine the effects of NO₂, a major component of air pollution, on airway eosinophilic inflammation and bronchial hyperreactivity, using a mouse model of asthma.

Setting and subjects: BALB/c mice (eight mice per experimental group) were studied in a basic research laboratory at the University of Iowa.

Interventions: Using a standard murine model of asthma, BALB/c mice were sensitized to ovalbumin (OVA) by intraperitoneal (IP) injections (days 1 and 7) and were challenged with aerosolized OVA (days 13 and 14). Some mice were exposed to NO₂ (2 ppm) in an exposure chamber for 24 h before undergoing OVA aerosol challenge. A control group was exposed to OVA alone.

Measurements and results: The outcomes assessed included airway inflammation, bronchial hyperreactivity to inhaled methacholine, and goblet cell hyperplasia. We found that NO₂ exposure modestly increased airway neutrophilia but not airway eosinophilia in OVA-exposed mice. These mice exhibited epithelial damage and loss of epithelial mucin. Surprisingly, nonspecific bronchial hyperreactivity (ie, enhanced pause index) was not increased, although baseline smooth muscle tone was increased (p < 0.05) in the mice exposed to NO₂.

Conclusions: These data indicate that relatively short-term (24 h) exposure to NO₂ causes epithelial damage, reduced mucin expression, and increased tone of respiratory smooth muscle. Reduced mucin production may be a mechanism of injury following long-term exposure to inhaled NO₂. Despite enhancing epithelial damage in OVA-exposed mice, NO₂ exposure does not otherwise alter the expression of allergen-induced airway responses.

Key Words: air pollution • environmental tobacco smoke • indoor air quality • mucin

This article has been cited by other articles:

				M. E. Poynter, R. L. Persinger, C. G. Irvin, K. J. Butnor, H. van Hirtum, W. Blay, N. H. Heintz, J. Robbins, D. Hemenway, D. J. Taatjes, et al. Nitrogen dioxide enhances allergic airway inflammation and hyperresponsiveness in the mouse Am J Physiol Lung Cell Mol Physiol, January 1, 2006; 290(1): L144 - L152. [Abstract] [Full Text] [PDF]