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A Reversible, Non-invasive Method for Airway Resistance Measurements and Bronchoalveolar Lavage Fluid Sampling in Mice
Published on: April 14, 2010
Ambient ozone concentrations induce airway hyperresponsiveness in some rat strains
P Depuydt1, G F Joos, R A Pauwels
1Dept of Respiratory Diseases, University Hospital, Ghent, Belgium.
The European Respiratory Journal
|September 18, 1999
Summary
Low-level ozone exposure triggers airway hyperresponsiveness (AHR) in specific rat strains without causing inflammation. Genetic factors likely explain these varied responses to ozone, impacting airway sensitivity.
Area of Science:
- Environmental toxicology
- Respiratory medicine
- Genetics
Background:
- Ozone exposure is a known cause of airway hyperresponsiveness (AHR).
- Previous animal studies utilized high ozone concentrations, yielding inconsistent findings.
- Variability in AHR response suggests underlying genetic influences.
Purpose of the Study:
- To investigate the impact of a single, low-level ozone exposure on AHR in various inbred rat strains.
- To determine if ozone-induced AHR is associated with airway inflammation.
- To explore the role of genetic factors in differential sensitivity to ozone.
Main Methods:
- Exposure of nine inbred rat strains to 0.05 ppm ozone for 4 hours.
- Assessment of airway responsiveness to 5-hydroxytryptamine (5-HT) intravenously.
- Analysis of bronchoalveolar lavage fluid (BALF) for inflammatory cells and markers.
Main Results:
- Lewis, BDII, and Long-Evans rats exhibited AHR 90 minutes post-exposure.
- Wistar, Sprague-Dawley, Fisher 344, Brown-Norway, BDE, and DA rats did not develop AHR.
- No significant inflammatory cell influx or elevation in BALF markers was observed in any strain.
- In Long-Evans rats, AHR persisted for up to 12 hours without inflammation indicators.
Conclusions:
- Ambient ozone concentrations can induce AHR in susceptible inbred rat strains.
- Ozone-induced AHR can occur independently of airway inflammation.
- Genetic background significantly influences individual susceptibility to ozone-induced AHR.

