Markers of eosinophilic and neutrophilic inflammation in bronchoalveolar lavage of asthmatic and atopic children

Authors


  • Edited by: Marc Humbert

Angelo Barbato Pediatric Pulmonology Unit, Department of Pediatrics, University of Padova, Via Giustiniani 3, 35128 Padova, Italy.
Tel.: +39 049 821 8015
Fax: +39 049 821 3502
E-mail: barbato@pediatria.unipd.it

Abstract

To cite this article: Snijders D, Agostini S, Bertuola F, Panizzolo C, Baraldo S, Turato G, Faggian D, Plebani M, Saetta M, Barbato A. Markers of eosinophilic and neutrophilic inflammation in bronchoalveolar lavage of asthmatic and atopic children. Allergy 2010; 65: 978–985.

Abstract

Background:  Recent studies performing fiberoptic bronchoscopy in children have improved our understanding of asthma pathophysiology. Eosinophilic, but also neutrophilic, inflammation has been described in asthma, but the relationship with atopy was incompletely investigated. The aim of this study is to examine inflammatory cells and mediators in children with asthma compared to the appropriate controls, i.e. atopic children without asthma and children with no atopy or asthma. Moreover, asthmatic children were analysed separately based on the presence of atopy and stratified by age.

Methods:  We recruited 191 children undergoing fiberoptic bronchoscopy for appropriate indications: 91 asthmatics (aged 1.4–17 years), 44 atopics without asthma (1.6–17.8 years) and 56 nonasthmatic nonatopic controls (1.4–14 years). In bronchoalveolar lavage, total and differential cell counts and inflammatory mediators, including ECP, eotaxin, IL-8 and TNFα, were analysed.

Results:  Eosinophils and ECP levels were increased in asthmatic children when compared to controls (P = 0.002 and P = 0.01, respectively), but also atopic children without asthma had increased ECP levels compared to controls (P = 0.0001). Among asthmatic children, eosinophils and ECP levels were not different between atopic and nonatopic individuals. Neither neutrophils nor the related mediators (IL-8 and TNFα) differed significantly in the three groups. This pattern of inflammation was observed in both preschool and school-aged asthmatic children.

Conclusions:  This study suggests that markers of eosinophilic, but not neutrophilic inflammation, are increased in asthmatic children and also in atopic children without asthma. Of interest, in asthmatic children, the activation of the eosinophilic response is not solely because of the presence of atopy.

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