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Copyright ©ERS Journals Ltd 2002
Rhinovirus infection in nonasthmatic subjects: effects on intrapulmonary airways
1 Depts of Pulmonology, 2 Medical Decision Making and 3 Virology, Leiden University Medical Center (LUMC), Leiden and 5 Dept of Pathology, St Radboud University Medical Center, Nijmegen, the Netherlands. 4 Respiratory Virus Research Laboratory, University of Wisconsin, Madison, WI, USA
CORRESPONDENCE: J. de Kluijver, Lung Function Laboratory, C2-P, Dept of Pulmonology, Leiden University Medical Center, Albinusdreef 2, PO Box 9600, NL-2300 RC, Leiden, The Netherlands. Fax: 31 715154691. E-mail: J.de_Kluijver@lumc.nl
Keywords: airway hyperresponsiveness, asthma, bronchial biopsies, intercellular adhesion molecule-1, virus infection
Received: May 23, 2001
Accepted February 20, 2002
This study was funded by "Stichting Astma Bestrijding", the Netherlands.
The common cold is a highly prevalent, uncomplicated upper airway disease. However, rhinovirus (RV) infection can lead to exacerbation of asthma, with worsening in airway hyperresponsiveness and bronchial inflammation. The current authors questioned whether such involvement of the intrapulmonary airways is disease specific.
Twelve nonatopic, healthy subjects (forced expiratory volume in one second (FEV1) >80% predicted, provocation concentration causing a 20% fall in FEV1 (PC20) >8 mg·mL–1) were experimentally infected with RV16. Next to PC20 and the maximal response to methacholine (MFEV1 and MV'40p), the numbers of mucosal inflammatory cells and epithelial intercellular adhesion molecule (ICAM)-1 expression in bronchial biopsies were assessed before and 6 days after RV16 inoculation.
RV16 infection induced a small but consistent increase in maximal airway narrowing, without a change in PC20. There was a significant increase in bronchial epithelial ICAM-1 expression after RV16, whereas inflammatory cell counts did not change. Nevertheless, the change in the number of submucosal CD3+ cells was correlated with the change in MV'40p.
In conclusion, rhinovirus infection in normal subjects induces a limited, but significant increase in maximal airway narrowing, which is associated with changes in bronchial T-cell numbers. Together with the upregulation of bronchial epithelial intercellular adhesion molecule-1, these findings indicate that, even in healthy subjects, rhinovirus infection affects the intrapulmonary airways.
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