4.4 Article

Rhinovirus is associated with severe asthma exacerbations and raised nasal interleukin-12

Journal

RESPIRATION
Volume 69, Issue 2, Pages 136-142

Publisher

KARGER
DOI: 10.1159/000056316

Keywords

rhinovirus; asthma; common cold; interleukin-10; interleukin-12

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Background. Rhinovirus (RV) is associated with asthma exacerbations in longitudinal studies, but the role in patients with acute severe asthma who require admission to a hospital emergency room remains to be fully defined. The cytokines interleukin-10 (IL-10) and IL-12 may be elevated or suppressed by viral infections and contribute to a worsening of airway inflammation in asthmatics. Objectives: We assessed the association of RV with acute severe asthma and nasal IL-10 and IL-12. Methods: Patients admitted to a hospital emergency asthma service had nasal aspirates (NAs) taken and peak expiratory flow (PEF) measured on admission and again 7, 28 and 56 days after admission. RV was sought in all NAB using a validated polymerase chain reaction assay and IL-10 and IL-12 were measured on admission and after 56 days in a subgroup of 22 asthmatics and 6 normal controls. Results: Thirty-seven asthmatics with a reduced PEF (% predicted) of 50.4 +/- 2.5% (mean +/- SEM) on admission were studied. RV was detected in NAB of 13 patients (35%) on admission, in 6 of the 13 patients after 7 days (16%), in 1 patient after 28 and 56 days and was absent in controls. IL-10 was not increased on admission or after 56 days. Measurements of IL-12 were raised on admission compared to 56 days later in asthmatics with RV detectable (p = 0.04). In asthmatics without RV, nasal IL-12 levels were correlated with PEF measurements over this period (r = 0.5, p < 0.05). Conclusions: A temporal relationship between the presence of nasal RV and emergency room admission for acute severe asthma was found in one third of patients. Low levels of IL-10 during RV infections could contribute to unopposed synthesis of pro-inflammatory cytokines whilst increases in IL-12 may amplify nasal and endobronchial inflammation. Copyright (C) 2002 S. Karger AG, Basel.

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