This project was supported by a grant from the FWO (Krediet aan Navorsers KNV I.5215.96 N) (G.F. Joos), and a grant from ECBiomed I (BMH1-CT94-1281) (R.A. Pauwels) and a grant from Astra Belgium. P. Depuydt received a Research Mandate of the Faculty Medicine of the University of Ghent.
Ambient ozone concentrations induce airway hyperresponsiveness in some rat strains
Article first published online: 25 DEC 2001
European Respiratory Journal
Volume 14, Issue 1, pages 125–131, July 1999
How to Cite
Depuydt, P. , Joos, G.F. and Pauwels, R.A. (1999), Ambient ozone concentrations induce airway hyperresponsiveness in some rat strains. European Respiratory Journal, 14: 125–131. doi: 10.1034/j.1399-3003.1999.14a21.x
- Issue published online: 25 DEC 2001
- Article first published online: 25 DEC 2001
- Airway hyperresponsiveness;
- airway inflammation;
Ozone is known to induce airway hyperresponsiveness (AHR) in humans and animals. Previous studies in animals used high exposure levels and reported inconsistent results. The aim of this study was to investigate the effect of a single low-level ozone exposure on different inbred rat strains.
Nine rat strains were exposed to 0.05 parts per million (ppm) for 4 h and airway responsiveness to intravenous 5-hydroxytryptamine (HT) examined. Bronchoalveolar lavage fluid (BALF) was examined for the presence of inflammatory cells and markers.
Lewis, BDII and Long-Evans rats developed AHR 90 min after ozone exposure, whereas Wistar, Sprague-Dawley, Fisher 344, Brown-Norway, BDE and DA rats did not. Baseline airway responsiveness to 5-HT differed significantly between rat strains, but did not correlate with the presence or absence of ozone-induced AHR. No inflammatory cell influx was found in BALF of any rat strain. In Long-Evans rats, AHR lasted up to 12 h after ozone exposure despite the absence of an inflammatory cell influx or increase in lactate dehydrogenase, alkaline phosphatase or total protein in BALF.
In conclusion, exposure to an ambient concentration of ozone induced airway hyperresponsiveness without airway inflammation in some highly inbred rat strains. Genetic factors are likely to account for the observed variability in sensitivity of the airways to ozone.