Source: Annual Congress 2006 - Virus-induced respiratory tract infection
Disease area: Airway diseases

Abstract

Rhinoviruses have been identified as the major viral triggers of asthma exacerbations. Recently it has been shown that asthma is an independent risk factor for invasive pneumococcal disease. Human neutrophil peptides (HNPs, α-defensins) play an important role in antimicrobial host defence and are induced by inflammation. We hypothesised that HNPs are induced by rhinovirus infections and deficient in asthmatics compared to normals. Asthmatic (10) and healthy volunteers (15) were experimentally infected by nasal application of rhinovirus 16. Asthmatic patients developed significantly increased lower respiratory tract symptoms and airflow obstruction, whereas these features were not induced in healthy controls. Before, four days and six weeks after infection, bronchoalveolar lavage was obtained in all subjects and SLPI (Secretory leucocyte protease inhibitor) and HNP 1-3 protein expression was determined in the supernatants. There was no induction of SLPI but HNP 1-3 levels in asthmatics were significantly higher during infection than convalescence (1.22 ng/ml vs. 0.45 ng/ml, p=0.0039). In healthy controls there was no induction. Experimental rhinovirus infection leads to an up-regulation of HNP 1-3 in asthmatics only. There were no differences between asthmatics and controls in HNP levels at any time point. These data do not support the hypothesis that deficient HNP levels in asthma are related to increased susceptibility to invasive pneumococcal disease.

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G. Rohde, S. D. Message, V. Laza-Stanca, P. Mallia, M. R. Edwards, S. L. Johnston (London, United Kingdom; Bochum, Germany). Increase in α-defensins during rhinovirus-induced experimental asthma exacerbations. Eur Respir J 2006; 28: Suppl. 50, 966

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