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Eosinophils in the pathogenesis of paediatric severe asthma

Saglani, Sejal; Lloyd, Clare M.

Current Opinion in Allergy and Clinical Immunology: April 2014 - Volume 14 - Issue 2 - p 143–148
doi: 10.1097/ACI.0000000000000045
PEDIATRIC ASTHMA AND DEVELOPMENT OF ATOPY: Edited by Carlos E. Baena-Cagnani and Leonard B. Bacharier

Purpose of review The importance and functional contribution of eosinophils to the pathogenesis of severe asthma was questioned when adult studies reported neutrophilic inflammation and Th17 cells were central to disease.

Recent findings Eosinophilic inflammation, atopic sensitization and airway remodelling are the hallmark features of severe asthma in children. Contrary to adult reports, neutrophils, Th17 and Th2 cytokines are rarely detected in children with severe disease who are prescribed high-dose steroids. Type 2 innate lymphoid cells (ILCs), which are induced by the epithelial cytokine interleukin (IL)-33, and also release the Th2 cytokines IL-5 and IL-13, have been shown to be important in mediating asthma, and specifically, ILCs have a role in mediating eosinophil homeostasis. A direct link between IL-33, airway remodelling and steroid resistance in paediatric severe asthma suggests the steroid-resistant eosinophilia may be mediated by ILCs rather than classical Th2 lymphocytes.

Summary Data from children with severe asthma have shown that findings from adults cannot be translated to children, and that steroid-resistant eosinophilic inflammation appears central to the pathogenesis of paediatric disease. Age-appropriate experimental models and use of airway samples from children are critical to understanding the underlying mechanisms and identifying novel therapeutic targets.

aLeukocyte Biology Section, National Heart & Lung Institute, Imperial College London

bDepartment of Respiratory Paediatrics, Royal Brompton Hospital, London, UK

Correspondence to Dr Sejal Saglani, Reader in Respiratory Paediatrics, 368 Sir Alexander Fleming Building, Imperial College London, Exhibition Road, London SW7 2AZ, UK. Tel: +44 2075943167; fax: +44 2075943119; e-mail:

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