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