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What do non-eosinophilic asthma and airway remodelling tell us about persistent asthma?

Correspondence to:
Professor Peter G Gibson, Level 3, Hunter Medical Research Institute, John Hunter Hospital, Locked Bag 1, Hunter Region Mail Centre, NSW 2310 Australia; peter.gibson@hnehealth.nsw.gov.au

The first 150 words of the full text of this article appear below.

Over a decade of careful clinicopathological investigation has characterised the allergen-triggered Th2 response in asthma that leads to eosinophilic airway inflammation. This research has directed drug discovery programmes and we now have effective treatment for most steps in the eosinophilic asthma pathway. This list includes interventions that act at discrete levels such as allergen avoidance, allergen immunotherapy, anti-IgE antibodies, anti-interleukin-5 monoclonal antibodies and leucotriene receptor antagonists, together with corticosteroids that act on multiple levels in the pathway. Despite this significant success in therapeutic discovery, asthma persists. There must be something more to the pathogenesis of asthma. What could it be?

Airway remodelling and non-eosinophilic asthma (NEA) are both topical answers to this question. To date these have been pursued as distinct entities, but the paper by Berry and colleagues¹ published in this issue of Thorax (see p 1043) addresses both issues and allows consideration of the . . . [Full text of this article]

Related Article

Pathological features and inhaled corticosteroid response of eosinophilic and non-eosinophilic asthma

Mike Berry, Angela Morgan, Dominick E Shaw, Deborah Parker, Ruth Green, Christopher Brightling, Peter Bradding, Andrew J Wardlaw, and Ian D Pavord
Thorax 2007 62: 1043-1049. [Abstract] [Full Text] [PDF]