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* Meakins Christie Laboratories, Department of Medicine, McGill University, Montreal, Quebec, Canada; and
Merck Frosst Centre for Therapeutic Research, Dorval, Quebec, Canada
PGE2 has been reported to inhibit allergen-induced airway responses in sensitized human subjects. The aim of this study was to investigate the mechanism of anti-inflammatory actions of PGE2 in an animal model of allergic asthma. BN rats were sensitized to OVA using Bordetella pertussis as an adjuvant. One week later, an aerosol of OVA was administered. After a further week, animals were anesthetized with urethan, intubated, and subjected to measurements of pulmonary resistance (RL) for a period of 8 h after OVA challenge. PGE2 (1 and 3 µg in 100 µl of saline) was administered by insufflation intratracheally 30 min before OVA challenge. The early response was inhibited by PGE2 (3 µg). The late response was inhibited by both PGE2 (1 and 3 µg). Bronchoalveolar lavage fluid from OVA-challenged rats showed eosinophilia and an increase in the number of cells expressing IL-4 and IL-5 mRNA. These responses were inhibited by PGE2. Bronchoalveolar lavage fluid levels of cysteinyl-leukotrienes were elevated after OVA challenge and were reduced after PGE2 to levels comparable with those of sham challenged animals. We conclude that PGE2 is a potent anti-inflammatory agent that may act by reducing allergen-induced Th2 cell activation and cysteinyl-leukotriene synthesis in the rat.
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