A COMMON COLD VIRUS, RHINOVIRUS-16, POTENTIATES AIRWAY INFLAMMATION AFTER SEGMENTAL ANTIGEN BRONCHOPROVOCATION IN ALLERGIC SUBJECTS

Citation
Wj. Calhoun et al., A COMMON COLD VIRUS, RHINOVIRUS-16, POTENTIATES AIRWAY INFLAMMATION AFTER SEGMENTAL ANTIGEN BRONCHOPROVOCATION IN ALLERGIC SUBJECTS, The Journal of clinical investigation, 94(6), 1994, pp. 2200-2208
Citations number
34
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Medicine, Research & Experimental
ISSN journal
0021-9738
Volume
94
Issue
6
Year of publication
1994
Pages
2200 - 2208
Database
ISI
SICI code
0021-9738(1994)94:6<2200:ACCVRP>2.0.ZU;2-Q
Abstract
Many patients with asthma have increased wheezing with colds. We hypot hesized that rhinovirus colds might increase asthma by augmenting airw ay allergic responses (histamine release and eosinophil influx) after antigen challenge. Seven allergic rhinitis patients and five normal vo lunteers were infected with rhinovirus type 16 (RV16) and evaluated by segmental bronchoprovocation and bronchoalveolar lavage. Segmental ch allenge with saline and antigen was performed 1 mo before infection, d uring the acute infection, and 1 mo after infection. Lavage was perfor med immediately and 48 h after antigen challenge. Data were analyzed b y two-way analysis of variance, and a P value of less than or equal to 0.05 was considered to be significant. All volunteers inoculated with RV16 developed an acute respiratory infection. BAL fluid obtained fro m allergic rhinitis subjects during the acute viral infection, and 1 m o after infection, showed the following significant RV16-associated ch anges after antigen challenge: (a) an enhanced release of histamine im mediately after local antigen challenge; (b) persistent histamine leak 48 h afterwards; and (c) a greater recruitment of eosinophils to the airway 48 h after challenge. These changes were not seen in non-allerg ic volunteers infected with RV16 and challenged with antigen, nor in a llergic volunteers repetitively challenged with antigen but not infect ed with RV16, nor in RV16 infected allergic volunteers sham challenged with saline. We conclude that rhinovirus upper respiratory infection significantly augments immediate and late allergic responses in the ai rways of allergic individuals after local antigen challenge. These dat a suggest that one mechanism of increased asthma during a cold is an a ccentuation of allergic responses in the airway which may then contrib ute to bronchial inflammation.