Riedel F, Krause A, Slenczka W, Rieger C H
Department of Paediatrics, Ruhr-University Bochum, Germany.
Clin Exp Allergy. 1996 May;26(5):603-9.
Viral respiratory tract infections have been previously considered to be associated with induction of allergic sensitization.
In order to investigate this relationship in an animal model, guinea-pigs were inoculated intranasally with Parainfluenza-3-(PI-3) virus (n = 16) or virus-free culture medium (controls, n = 12), sensitized at day 4 with inhaled ovalbumin (OA) and challenged 3 weeks later with inhaled OA using specific bronchial provocation testing with body plethysmographic measurement of compressed air (CA). Furthermore, specific anti-OA-IgG1-antibodies in serum before challenge were determined by enzyme linked immunosorbent assay (ELISA). For investigation of airway epithelium permeability horseradish peroxidase (HRP) was inhaled at day 4 after inoculation by six animals, and HRP serum concentrations were determined by a direct ELISA 30 min after inhalation.
PI-3 infected animals were found to be significantly more sensitized to OA compared with controls, with higher CA values (P < 0.001) on specific bronchial provocation and with increased specific anti-OA-IgG1 titers. Serum-HRP concentrations were about 20 times higher in the infected animals compared with controls. PI-3 infected and sham-infected animals had comparable bronchial reactions on specific provocation with OA when sensitized systemically.
We conclude that viral respiratory tract infection with PI-3 virus enhances inhalative allergic sensitization in the guinea-pig. Increased mucosal permeability to antigens may be an important pathophysiological mechanism.
