Asthma is an extremely common illness which affects an estimated 300 million people of all ages and ethnic backgrounds worldwide with significant costs for healthcare systems.¹ The clinical course of the disease is characterised by acute episodes of worsening of symptoms and decrease in lung function known as exacerbations. Prevention of exacerbations has been the goal of most therapeutic interventions developed so far because exacerbations seriously affect the quality of life of patients and their families.² The clinical presentation of asthma exacerbations may be extremely heterogeneous; they can be rapid in onset or occur more gradually. The severity of asthma exacerbations is also extremely variable, ranging from mild episodes to severe attacks which result in respiratory failure and may ultimately lead to death.

Airway inflammation is a characteristic feature consistently present in patients with asthma from the early stages in children³ to elderly people.⁴ The inflammatory process has been extensively investigated in stable conditions, showing an increased infiltration of eosinophils, mast cells and CD4 T lymphocytes characterised by a Th2 profile, with release of cytokines such as interleukin (IL)-4, IL-5, IL-13, eotaxin and RANTES.⁵ Conversely, little is known about the cellular mechanisms activated during exacerbations and, in particular, in severe exacerbations.

In this issue of Thorax …