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Departments of 1 Medicine and 2 Pathology, Vanderbilt University Medical Center, Nashville, Tennessee 37232
PGE2 is an important cyclooxygenase product
that modulates airway inflammatory and smooth muscle responses. Signal
transduction is mediated by four EP receptor subtypes that cause
distinct effects on cell metabolism. To determine the role of
EP2 receptor activation, we produced a mouse lacking the
EP2 receptor by targeted gene disruption. The effect of
aerosolized PGE2 and other agonists was measured using
barometric plethysmography and by measurements of lung resistance in
mechanically ventilated mice. Inhalation of PGE2 inhibited
methacholine responses in wild-type but not in mice lacking the
EP2 receptor
[EP2(
/)]. After airway
constriction was induced by methacholine aerosol, PGE2
reduced the airway constriction enhanced pause in wild-type mice (from
0.88 ± 0.15 to 0.55 ± 0.06) but increased it in
EP2(/) mice (from 0.73 ± 0.08 to 1.27 ± 0.19). Similar results were obtained in mechanically ventilated mice.
These data indicate that the EP2 receptor mediates the
bronchodilation effect of PGE2.
pharmacology; airway reactivity; methacholine; knockout mice
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