The Effect of Parainfluenza 3 Infection on Guinea Pig Basophil and Lung Mast Cell Histamine Release

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Abstract
The guinea pig infected with parainfluenza 3 (P-3) has provided an animal model to study mechanisms of virus-induced asthma and airway hyperreactivity. Evidence to identify the mechanism by which P-3 infection enhances airway hyperractivity, however, has not been established. The present study evaluated the effect of P-3 infection on histamine release (HR) from isolated peripheral blood guinea pig basophils and lung mast cells. Basophil HR was determined in animals made basophilci with 13 daily intraperitoneal injections of sheep blood. On Day 10 of the sensitization, blood was obtained from all animals, and leukocyte HR was determined to sheep gammaglobulin (SG), which served as the secretagogue. After these baseline studies, the animals were separated into two groups; one was insufflated with P-3 virus and other with growth medium that did not contain virus. Four days later, animals were killed, basophils and lung mast cells were isolated, HR were determined, and lung tissue was cultured for the presence of virus. In basophils isolated from animals proven to be infected with P-3 virus, we found significantly more histamine released in response to the lower doses of SG and a significant shift in the -log EC50 dose of this antigen causing HR in these cells. Experiments conducted with the calcium ionophore A23187 as the basophil secretagogue in the same experimental design did not demonstrate similar HR findings. Furthermore, a defect in calcium disposition did not account for the enhanced HR from basophils isolated from infected animals. HR from pulmonary mast cells was similar in cells isolated from P-3-infected and control insufflated animals. Our results indicate that basophils isolated from P-3-infected guinea pigs have enhanced HR to immunologically dependent stimuli and, furthermore, that this heightened secretory response is not found in lung mast cells. We posulate a possible P-3 virus effect specific for basophils leading to greater mediator release and raise the question of basophil participation in mechanisms that cause increased airway reactivity in P-3-infected guinea pigs.