Asthma is chronic inflammatory disease of the airways characterized by variable and reversible airflow obstruction. The symptoms of asthma include shortness of breath, cough, chest tightness and wheezing. Genetic factors are thought to play an important role in the development of the disease, however the phenotype expression is profoundly affected by environmental factors1. Asthma affects 334 million people all over the world and is the most common chronic disease among children2. In the UK alone, 5.4 million people suffer from asthma of which 4.3 million adults and 1.1 million children. The UK has among the highest prevalence rates of asthma worldwide in adults (1 in 12) and particularly in children (1 in 11). As a result, the NHS spends
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Asthma is increasingly recognised has a syndrome rather than a disease. This implies that asthma is an umbrella term describing different asthmatic phenotypes with similar symptoms that are each associated to distinct pathophysiologic and pathogenetic mechanisms, known as endotypes8. Much research has focused on the different inflammatory phenotypes of asthma. It was initially thought that asthma was an allergic, Th2 mediates eosinophilic airway inflammatory disease. However, this phenotype is only one of the inflammatory phenotypes and at least four others have been recognised: non-allergic eosinophilic, neutrophilic, mixed eosinophilic and neutrophilic and paucigranulocytic inflammatory phenotypes8. These differences in inflammatory phenotypes could in part explain why corticosteroids fail to control asthma exacerbations in many patients. Nevertheless, patients with similar inflammatory phenotypes still exhibit differences in terms of other criteria used to classify asthma and in particular in terms of responsiveness to treatment (severity of exacerbations)8. As a result, the classification of asthma remains disputed and patients continue to be treated in function of the severity of their symptoms rather than the aetiology of the disease. This for instance demonstrates the wide gap between the clinical and the experimental understanding of the
Asthma is increasingly recognised has a syndrome rather than a disease. This implies that asthma is an umbrella term describing different asthmatic phenotypes with similar symptoms that are each associated to distinct pathophysiologic and pathogenetic mechanisms, known as endotypes8. Much research has focused on the different inflammatory phenotypes of asthma. It was initially thought that asthma was an allergic, Th2 mediates eosinophilic airway inflammatory disease. However, this phenotype is only one of the inflammatory phenotypes and at least four others have been recognised: non-allergic eosinophilic, neutrophilic, mixed eosinophilic and neutrophilic and paucigranulocytic inflammatory phenotypes8. These differences in inflammatory phenotypes could in part explain why corticosteroids fail to control asthma exacerbations in many patients. Nevertheless, patients with similar inflammatory phenotypes still exhibit differences in terms of other criteria used to classify asthma and in particular in terms of responsiveness to treatment (severity of exacerbations)8. As a result, the classification of asthma remains disputed and patients continue to be treated in function of the severity of their symptoms rather than the aetiology of the disease. This for instance demonstrates the wide gap between the clinical and the experimental understanding of the