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Interleukin‐1β and interleukin‐1ra levels in nasal lavages during experimental rhinovirus infection in asthmatic and non‐asthmatic subjects
Author(s) -
De Kluijver J.,
Grünberg K.,
Pons D.,
De Klerk E. P. A.,
Dick C. R.,
Sterk P. J.,
Hiemstra P. S.
Publication year - 2003
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1046/j.1365-2222.2003.01770.x
Subject(s) - rhinovirus , budesonide , medicine , asthma , placebo , immunology , inflammation , basal (medicine) , interleukin , gastroenterology , respiratory system , cytokine , pathology , alternative medicine , insulin
Summary Background Exacerbations of asthma are often associated with rhinovirus (RV)‐induced common colds. During experimental RV‐infection in healthy subjects, increased levels of the pro‐inflammatory mediator IL‐1β and the anti‐inflammatory IL‐1 receptor antagonist (IL‐1ra) have been found in nasal lavage . Objective We postulated that the balance between nasal pro‐ and anti‐inflammatory mediator expression is disturbed in asthma, resulting in more extensive inflammation following RV‐exposure in asthma. Methods We determined IL‐1ra, IL‐1β, and IL‐8 in nasal lavages (days −2, 3, and 6) of non‐asthmatics and asthmatics (with and without pre‐treatment with the inhaled steroid budesonide) before and after experimental RV16‐infection (days 0 and 1). Results Following RV16‐infection, a significant increase in IL‐8 was observed in the placebo‐ and budesonide‐treated asthmatics ( P =0.033 and 0.037, respectively), whereas IL‐1β only increased in the two asthma groups combined ( P =0.035). A small, but significant, increase in IL‐1ra was only observed in the budesonide‐treated asthmatics ( P =0.047). At baseline, IL‐1ra levels were significantly higher in the non‐asthmatics than in the placebo‐treated asthmatics ( P =0.017). Conclusion These results demonstrate differences between non‐asthmatic and asthmatic subjects in the basal levels of nasal cytokines and their inhibitors, and in the effect of experimental RV‐infection on these levels. The results indicate that RV may enhance inflammation more markedly in asthmatics, and suggest that this may in part be explained by lower IL‐1ra levels. In addition, the observation that budesonide‐treatment may result in higher nasal IL‐1ra levels supports the hypothesis that steroids act in part by increasing the endogenous anti‐inflammatory screen.