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Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
Published on: August 25, 2017
Breathing and pulmonary surfactant function in mice 24 h after ozone exposure
W D Currie1, S van Schaik, I Vargas
1Dept of Radiology, Duke University Medical Center, Durham, NC, USA.
The European Respiratory Journal
|September 4, 1998
Summary
Acute ozone exposure impairs breathing and lung surfactant function in mice. Inflammatory proteins in the airways reduce surfactant
Area of Science:
- Environmental Health
- Pulmonary Physiology
- Toxicology
Background:
- Ozone is a major air pollutant with known respiratory effects.
- Pulmonary surfactant is crucial for maintaining airway patency.
- The impact of acute ozone exposure on surfactant function is not fully understood.
Purpose of the Study:
- To investigate the effects of acute ozone exposure on respiratory parameters.
- To assess the functional capacity of pulmonary surfactant after ozone inhalation.
- To identify mechanisms underlying ozone-induced airway dysfunction.
Main Methods:
- BALB/c mice exposed to 1 ppm ozone for 2-8 hours.
- Respiratory function assessed via plethysmography.
- Bronchoalveolar lavage (BAL) fluid analyzed for inflammatory cells, proteins, and phospholipids.
- Surfactant function evaluated using a capillary surfactometer (CS).
Main Results:
- Ozone exposure significantly increased respiratory frequency and decreased tidal volume.
- Surfactant dysfunction was observed, despite increased phospholipid levels.
- Elevated protein concentrations in BAL fluid correlated with surfactant dysfunction.
- Washing the surfactant restored its normal function, indicating protein inhibition.
Conclusions:
- Acute ozone exposure causes breathing alterations and airway inflammation in mice.
- Inflammatory proteins in the airways inhibit pulmonary surfactant function.
- This inhibition compromises the surfactant's role in maintaining airway patency.
