Source: Annual Congress 2002 - Bronchiolitis
Disease area: Airway diseases, Paediatric lung diseases

Abstract

Background: RSV infection is the major cause of viral respiratory illness in children throughout the world. Longterm sequelae of RSV bronchiolitis include wheeze and asthma. Recently,the Th2 cytokine Interleukin-9 (IL-9) has been implicated in the pathogenesis of asthma ¹. IL-9 causes the development of lung eosinophilia, mucus hypersecretion and bronchial hyper-responsiveness. It also induces the expression of other Th2 cytokines and chemokines. Our study examined IL-9 mRNA expression and protein levels in severe RSV bronchiolitis.
Methods: 120 serial non-bronchoscopic bronchoalveolar lavages (BAL) were performed on 27 infants ventilated for RSV-positive bronchiolitis. Control BALs were performed on 7 infants ventilated for non-infective non-respiratory causes.IL-9 expression was determined using an RNase protection assay. We have developed an IL-9 ELISA and have used this to determine protein concentration.
Results: All patients were <1 year; median age 11 weeks; underlying pathology in 19/27 (prematurity in 16/19); median ventilation time 5 days. IL-9 mRNA was detected in 22/27 infants ventilated with RSV bronchiolitis (mean IL-9/GAPDH ratio, 1.57 +/- 0.98) and in none of the control patients. Il-9 protein was detected in 24/27 patients (mean IL-9 concentration, 1595 +/- 1493 pg/ml) and in none of the control patients.
Conclusions: IL-9 mRNA and protein are present in BAL from infants with severe RSV bronchiolitis. This cytokine may play a role in the disease pathogenesis of RSV bronchiolitis as well as asthma.
References
1. Soussi-Gounni A, Kontolemos M, Hamid Q. Role of IL-9 in the pathophysiology of allergic diseases. J Allergy Clin.Immunol. 2001;107(4):575-82.

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Citations should be made in the following way:
P. S. McNamara, P. C. Ritson, B. F. Flanagan, C. A. Hart, R. L. Smyth (Liverpool, United Kingdom). Interleukin-9 in severe respiratory syncytial virus (RSV) bronchiolitis. Eur Respir J 2002; 20: Suppl. 38, 240

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