Rhinovirus-16 colds in healthy and in asthmatic subjects - Similar changesin upper and lower airways

Citation
He. Fleming et al., Rhinovirus-16 colds in healthy and in asthmatic subjects - Similar changesin upper and lower airways, AM J R CRIT, 160(1), 1999, pp. 100-108
Citations number
37
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
ISSN journal
1073449X → ACNP
Volume
160
Issue
1
Year of publication
1999
Pages
100 - 108
Database
ISI
SICI code
1073-449X(199907)160:1<100:RCIHAI>2.0.ZU;2-E
Abstract
Rhinovirus (RV) infections appear to precipitate most asthma exacerbations. To investigate whether RV-16 induces different inflammatory changes in upp er and lower airways of asthmatic and healthy subjects, we inoculated 10 no natopic healthy and 11 atopic asthmatic adults with 2,000 TCID50 RV-16. Sub jects recorded symptoms and peak flow daily; and they underwent spirometry, methacholine challenge (PC20), nasal lavage, and sputum induction at basel ine and on Days 2, 4, 15, and 29 d after inoculation. One asthmatic subject developed an exacerbation requiring prednisone treatment 5 d after inocula tion. The cold symptom severity (Jackson score) did not differ between grou ps. During the cold, asthma symptoms increased slightly from baseline in th e asthmatic group; and PC20 decreased in the healthy group. However, peak f low, bronchodilator use, and spirometry did not change in either group. At baseline, asthmatics had higher neutrophils, eosinophils, and interleukin ( IL)-6 in nasal lavage. After inoculation, both groups developed significant increases in nasal neutrophils, IL-6 and IL-8, and modest increases in spu tum neutrophils and IL-6, but not IL-8. However, these changes did not diff er between groups. IL-5, interferon-gamma, and RANTES were detected only in nasal lavages from two asthmatic subjects, who had the most severe colds. IL-11 was not detected in any sample. We conclude that inflammatory respons es of upper and lower airways during RV-16 colds are similar in asthmatic a nd healthy subjects, and that RV-16 infection is not by itself sufficient t o provoke clinical worsening of asthma.