MECHANISMS OF BRONCHOCONSTRICTION AFTER ALLERGEN INGESTION IN SENSITIZED GUINEA-PIGS

We examined whether oral administration of allergen induced bronchoconstriction in sensitized guinea pigs and investigated the mechanisms of bronchoconstriction. The animals had been immunized intraperitoneally with a mixture of Ascaris suum extract and silica gel, and exposed to ozone. They were then challenged with an oral dose of A. suum extract (6 mg/kg), and respiratory resistance (Rrs) was measured up to 7 h. After oral administration of the allergen, an increase in Rrs was observed. The mean values at 1, 3,5 and 7 h after oral allergen challenge were 150 +/- 21, 149 +/- 11, 151 +/- 12 and 134 +/- 10% of the baseline value, respectively. When saline instead of the allergen was orally administered, almost no significant increase in Rrs was observed up to 7 h. Moreover, in nonsensitized guinea pigs, oral administration of allergen produced no significant increase in Rrs for up to 7 h. When atropine was administered as an aerosol, the increase in Rrs induced by an oral allergen challenge was attenuated. Three of the five atropine-treated guinea pigs showed temporary increases in Rrs immediately after the oral allergen challenge. The mean values of Rrs in the atropine-treated animals challenged with oral allergen at 1, 3, 5 and 7 h were 106 +/- 3, 106 +/- 5, 115 +/- 5 and 102 +/- 4% of baseline value, respectively. In the animals which received oral allergen, the number of neutrophils in bronchoalveolar lavage fluid (BALF) significantly increased 2.0-fold (p < 0.05), while no significant increase in the number of eosinophils, macrophages, or lymphocytes in BALF was observed. We conclude that oral allergen challenge can induce bronchoconstriction associated with neutrophilia in BALF in sensitized guinea pigs, and that vagal reflex pathways play a role in bronchoconstriction.