PARAINFLUENZA-3-VIRUS INFECTION ENHANCES ALLERGIC SENSITIZATION IN THE GUINEA-PIG

Citation
F. Riedel et al., PARAINFLUENZA-3-VIRUS INFECTION ENHANCES ALLERGIC SENSITIZATION IN THE GUINEA-PIG, Clinical and experimental allergy, 26(5), 1996, pp. 603-609
Citations number
17
Categorie Soggetti
Allergy,Immunology
ISSN journal
09547894
Volume
26
Issue
5
Year of publication
1996
Pages
603 - 609
Database
ISI
SICI code
0954-7894(1996)26:5<603:PIEASI>2.0.ZU;2-8
Abstract
Background Viral respiratory tract infections have been previously con sidered to be associated with induction of allergic sensitization. Obj ective and Methods In order to investigate this relationship in an ani mal model, guinea-pigs were inoculated intranasally with Parainfluenza -3-(PI-3) virus (n = 16) or virus-free culture medium (controls, n = 1 2), sensitized at day 4 with inhaled ovalbumin (OA) and challenged 3 w eeks later with inhaled OA using specific bronchial provocation testin g with body plethysmographic measurement of compressed air (CA). Furth ermore, specific anti-OA-IgG1-antibodies in serum before challenge wer e determined by enzyme linked immunosorbent assay (ELISA). For investi gation of airway epithelium permeability horseradish peroxidase (HRP) was inhaled at day 4 after inoculation by six animals, and HRP serum c oncentrations were determined by a direct ELISA 30 min after inhalatio n. Results PI-3 infected animals were found to be significantly more s ensitized to OA compared with controls, with higher CA values (P<0.001 ) on specific bronchial provocation and with increased specific anti-O A-IgG1 titers. Serum-HRP concentrations were about 20 times higher in the infected animals compared with controls. PI-3 infected and sham-in fected animals had comparable bronchial reactions on specific provocat ion with OA when sensitized systemically. Conclusions We conclude that viral respiratory tract infection with PI-3 virus enhances inhalative allergic sensitization in the guinea-pig. Increased mucosal permeabil ity to antigens may be an important pathophysiological mechanism.