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A Reversible, Non-invasive Method for Airway Resistance Measurements and Bronchoalveolar Lavage Fluid Sampling in Mice
Published on: April 13, 2010
EP(2) receptor mediates bronchodilation by PGE(2) in mice
J R Sheller1, D Mitchell, B Meyrick
1Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA. James.Sheller@MCMail.Vanderbilt.edu
Journal of Applied Physiology (Bethesda, Md. : 1985)
|June 14, 2000
Summary
Prostaglandin E2 (PGE2) causes airway relaxation via the EP2 receptor. Mice lacking the EP2 receptor showed increased airway constriction when treated with PGE2, indicating its crucial role in bronchodilation.
Area of Science:
- Respiratory medicine
- Pharmacology
- Immunology
Background:
- Prostaglandin E2 (PGE2), a cyclooxygenase product, influences airway inflammation and smooth muscle function.
- Four EP receptor subtypes mediate PGE2's signaling, each with distinct cellular effects.
Purpose of the Study:
- To investigate the specific role of the EP2 receptor in mediating the effects of PGE2 on airway responses.
- To determine if EP2 receptor activation is responsible for PGE2-induced bronchodilation.
Main Methods:
- Generation of EP2 receptor-deficient mice (EP2-/-) using targeted gene disruption.
- Assessment of airway responses to inhaled PGE2 and methacholine using barometric plethysmography.
- Measurement of lung resistance in mechanically ventilated wild-type and EP2-/- mice.
Main Results:
- PGE2 inhalation inhibited methacholine-induced airway constriction in wild-type mice.
- This inhibitory effect of PGE2 was absent in EP2-/- mice.
- Conversely, PGE2 exacerbated airway constriction in EP2-/- mice, suggesting a critical role for EP2.
Conclusions:
- The EP2 receptor is the primary mediator of PGE2-induced bronchodilation.
- Targeting the EP2 receptor may offer a therapeutic strategy for managing airway hyperresponsiveness.
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