Abstract
Asthma is a heterogenous chronic inflammatory airway disease comprising of four phenotypes classified based on sputum cytology, which differ in immunopathophysiology, disease severity, and response to pharmacological therapy. The phenotypes of asthma include eosinophilic, neutrophilic, paucigranulocytic, and mixed cellularity. Eosinophilic asthma affects about 40-60% of all asthma cases. It is associated with atopy, eczema, allergic rhinitis, aspirin exacerbated respiratory disease, and chronic rhinosinusitis with nasal polyps. The airway epithelium plays an important role in initiating eosinophilic inflammation, and in the pathogenesis of eosinophilic asthma. Injured or damaged airway epithelium release three cytokines, such as interleukin-25 (IL-25, IL-33, and thymic stromal lymphopoietin (TSLP). Epithelial cytokines also known as alarmins act in concert and synergistically in promoting eosinophilic inflammation, airway hyperresponsiveness, and remodeling. Targeted inhibition of epithelial cytokines is an attractive and precise approach to treat eosinophilic asthma. There are no approved biologics targeting IL-25, and IL-33 for the treatment of eosinophilic asthma. Tezepelumab an anti-TSLP monoclonal antibody is the only anti-alarmin biologic approved for the treatment of severe asthma irrespective of the phenotype. It is effective in reducing the exacerbation rates, and improves lung function, and health related quality of life.