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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
Lymphokine-induced airway hyperresponsiveness in the rat
1Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada.
Insights
Interleukin-2 (IL-2) administration in rats significantly increased airway hyperresponsiveness and inflammation. Lymphocyte release of IL-2 may mediate airway hyperresponsiveness in chronic airway diseases.
Area of Science:
- Immunology
- Pulmonology
- Cell Biology
Background:
- Chronic airway inflammation is a hallmark of conditions like asthma.
- Lymphocytes and lymphokines, such as interleukin-2 (IL-2), play a role in immune responses.
- The specific contribution of lymphocytes to airway hyperresponsiveness requires further elucidation.
Purpose of the Study:
- To investigate the role of lymphocytes in chronic airway inflammation and responsiveness.
- To determine if interleukin-2 (IL-2) administration affects airway responsiveness and inflammation in rats.
Main Methods:
- Lewis rats were administered either IL-2 or a vehicle subcutaneously twice daily for 4.5 days.
- Pulmonary resistance and airway responsiveness to methacholine (MCh) were measured.
- Lung lavage was performed, and lung histology was assessed for edema and cellular infiltration.
Main Results:
- IL-2 administration significantly increased airway responsiveness to MCh (p = 0.001).
- IL-2 increased total cells, lymphocytes, neutrophils, and eosinophils in lung lavage.
- Histological analysis revealed IL-2-induced edema and mixed cellular infiltration, with lymphocytes predominating around airways and veins.
Conclusions:
- Interleukin-2 (IL-2) administration exacerbates airway hyperresponsiveness and inflammation in a rat model.
- A correlation exists between airway responsiveness and airway inflammation.
- Lymphocyte-derived IL-2 may be a key mediator in the pathogenesis of airway hyperresponsiveness.
Abstract:
We evaluated the potential role of the lymphocyte in chronic airway inflammation and responsiveness by repeated administration to rats of interleukin-2 (IL-2), the principal lymphokine responsible for lymphocyte proliferation. Lewis rats (mean weight, 184 +/- 2 g) received either 120,000 units of IL-2 (n = 10) or vehicle (n = 7) subcutaneously twice a day for 4.5 days. Animals were anesthetized with urethane and intubated for measurements of pulmonary resistance (RL) and airway responsiveness to aerosol methacholine (MCh). Lung lavage was performed, the animals were exsanguinated, and the lungs were fixed in 10% formalin. Histologic edema and the extent of infiltration of the bronchi, pulmonary veins, and arteries by cells was scored blindly. IL-2 increased airway responsiveness to MCh; the concentrations of MCh causing a doubling of RL were 0.14 versus 1.39 mg/ml (geometric mean) for the IL-2 and vehicle group, respectively (p = 0.001). IL-2 significantly increased total cellular return and the percentage of lymphocytes, neutrophils, and eosinophils in lavage. IL-2 caused edema and a mixed cellular infiltration of the bronchovascular tree. Lymphocytes predominated around the airways and veins. A correlation (r = 0.50) was present between airway responsiveness and airway inflammation but not with edema or vascular infiltration. Release of IL-2 by lymphocytes in the airways may be an important mediator of airway hyperresponsiveness.
