Figure 2From: Activity of the cyclooxygenase 2-prostaglandin-E prostanoid receptor pathway in mice exposed to house dust mite aeroallergens, and impact of exogenous prostaglandin E2Endogenous prostaglandin production in the airways as assayed by ELISA in BAL fluid. Graph (a) shows endogenous PGE2 production. PGE2 increased 2.4 fold in allergen-sensitized (n = 11) versus non-sensitized mice (n = 5). Endogenous PGE2 production fell significantly to baseline levels in HDM-sensitized mice treated with PGE2 (n = 11), but remained unchanged when mice were treated with sulprostone (n = 11). Graph (b) depicts endogenous airway 6-keto PGF1α production (a metabolite of PGI2). In the same way as PGE2, 6-keto PGF1α increased 2.4 fold in allergen-sensitized (n = 11) versus non-sensitized mice (n = 5). 6-keto PGF1α production fell in HDM-sensitized mice treated with PGE2 (n = 11) and sulprostone had a similar inhibitory effect on BAL 6-keto PGF1α expression (n = 11). Graph (c) shows endogenous PGD2 production. No differences were found in BAL fluid levels of PGD2 in mice between any of the experimental groups (*p < 0.05, **p < 0.01, ***p < 0.005).Back to article page