Ascaris suumOva-induced Bronchoconstriction, Eosinophilia, and IgE Antibody Responses in Experimentally Infected Primates Did Not Lead to Histamine Hyperreactivity

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Abstract
The hypothesis that active immunization of primates to give airway allergic responses would also confer on them a hyperreactivity to a nonspecific stimulus such as histamine was tested in 29 normal rhesus primates. At 6 wk after immunization, specific primate IgE (Rast) to Ascaris antigen had increased from 0.35 ± 0.17 to 0.98 ± 0.35 units/ml × 102 (p < 0.05). Histamine released from bronchial alveolar lavage cells in response to antigen increased from 5.4 ± 0.67 to 24 ± 1.8ng/106 cells (p < 0.05). In a subgroup of seven animals, airway resistance Rl and compliance before and after feeding embryonated Ascaris ova increased from Rl 3.5 ± 3.1 to 275 ± 212 cm H2O/L/s (p = 0.02) and Cdyn fell from 81 ± 10 to 11.3 ± 12 ml/cm H2O (p < 0.05). The bronchial lavage fluid contained a very high percentage of eosinophils after infection, 8 ± 3.1 to 24 ± 13% per 500 cells counted, and did not increase appreciably upon later antigen challenge, 24 ± 13 to 31 ± 11% of the cells at 9.5 h after antigen challenge (p = NS). When a group of seven of these 29 animals were compared for their histamine responsiveness before and after acquired Ascaris airway reactivity, there was no difference in 19 animals. Pulmonary response to histamine delivered from freon canisters at doses of 0.005, 0.01, 0.025, and 0.05% did not change (Rl, 141 ± 102 to 93 ± 62; Cdyn, 49 ± 7 to 46 ± 11% change before and after, respectively) (p = NS). Therefore, the hypothesis that active immunization leads to increased reactivity to nonspecific stimuli does not hold for the primate pulmonary model of airway diseases.