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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 interaction and overlap between airway remodelling and inflammatory subtype in asthma.
NEA refers to an asthma subtype where patients exhibit asthma symptoms and abnormal airway physiology (airway hyperresponsiveness (AHR), variable airflow obstruction) in the absence of a significant airway eosinophilia.2 Its importance arises because NEA is common, it seems to have a different pathogenesis from allergen-induced asthma3 and it may be relatively resistant to corticosteroid therapy.4
Airway remodelling in asthma refers to changes in structural components of the airway wall and is believed to result in fixed airflow obstruction, persistent AHR and a poor …
Competing interests: None.
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