Dear Colleagues,

Asthma remains a major cause of ill-health worldwide that presents as a chronic inflammatory airways disorder characterized by a clinical picture ranging from very mild and occasional symptoms to recurrent significant exacerbations that may, in a small number of patients, have a fatal or near-fatal outcome, thereby representing a clear unmet medical need. Asthma represents a complex and heterogeneous disease with diverse inflammatory events that lead to structural and functional changes in the lungs, including goblet cell hyperplasia, airway smooth muscle hypertrophy and sub-epithelial fibrosis in the airways that in turn give rise to airway hyperresponsiveness (AHR) and reversible airflow limitation. The processes that underlie asthma are characterised by different patterns of cytokine-based inflammation involving diverse cell types, such as T cells, B cells, mast cells, eosinophils, basophils, neutrophils and dendritic cells, as well as structural cell types including epithelial, smooth muscle and mesenchymal cells. Asthma can be divided into ‘asthma phenotypes’ that take demographic, clinical and/or pathophysiological characteristics into account. A further refinement involves division into disease entities termed ‘asthma endotypes’ based on specific pathophysiological mechanisms. For example, T helper 2 (TH2)-high asthma is seen in around 50% of patients who typically have eosinophilic inflammation mediated by cytokines including IL-4, IL-5 and IL-13. Elevated levels of immunoglobulin E (IgE) may also be present, while both Th2 and non-Th2 mechanisms contribute to asthma pathogenesis. Furthermore, respiratory viral infection is known to be a common risk factor for asthma exacerbations, where the underlying mechanisms need to be elucidated. The majority of asthmatic patients achieve satisfactory symptom control using inhaled glucocorticosteroids (GCs) and bronchodilators such as β2-adrenergic agonists, with the addition of oral leukotriene inhibitors if required. However, severe disease is seen in the approximately 5% of asthmatic subjects who do not achieve satisfactory asthma control despite adherence to high-dose inhaled or systemic glucocorticoid therapies, giving rise to recurrent exacerbations and persistent symptoms together with significant morbidity and quality of life issues, with attendant health cost implications.

The elucidation of the complex patterns of inflammation underlying asthma pathogenesis has informed the development of monoclonal-antibody-based biologic therapies that target the type 2 cytokines IL-4, IL-5 and IL-13 or IgE. It is increasingly accepted that significant clinical effects with anti-cytokine-based biologic therapies are more likely in carefully selected patient populations that take asthma phenotypes into account, which in turn rely on straightforward discriminatory biomarkers to aid the targeting of those most likely to benefit from treatment with these expensive interventions. This Special issue of Cells will address key aspects of the pathogenesis of asthma that inform the diagnosis and treatment of this condition, together with the development of more effective novel therapies for this important and common condition.

Dr. Garry M. Walsh
Dr. De-Yun Wang
Guest Editors

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• asthma
• severe asthma
• allergen immunotherapy
• co-morbidities
• COVID-19
• rhinitis
• obesity
• viral infection
• T cells
• mast cells
• eosinophils
• neutrophils
• epithelial cells
• smooth muscle cells
• glucocorticosteroids
• biomarkers
• biologics
• IgE
• IL4/13
• IL-5