Asthma is a common but complex chronic inflammatory heterogeneous lung disease, punctuated by the pathophysiological phenomenon of airway narrowing, coupled with symptoms of wheezing and coughing. The mechanism behind these symptoms is due to migration of eosinophils, mast cells, and CD4 T-helper cells into the submucosa of the airway, leading to hyperresponsiveness to common allergens, microorganisms, oxidants, pollutants, and consequently, airway remodeling. There is evidence that this migration is mediated by inflammatory cytokines derived from T-helper 2 (Th2) cells and type 2 innate lymphoid cells (ILC2), such as interleukins 4, 5, and 13. These cytokines lead to an increase in immunoglobulin E (IgE) production. Additionally, thymic stromal lymphopoietin (TSLP) released from airway epithelium can activate Th2 cells, innate lymphoid cells, or both. All have proven significant in the promotion of chronic airway inflammation and remodeling. In the past, most treatment strategies for this condition focused on two drug classes: β2 agonists (both short- and long-acting), and inhaled corticosteroids. Other treatments have included maintenance drugs, such as leukotriene receptor antagonists, long-acting anticholinergic agents, and theophylline. None of these, however, directly impact the interleukin or IgE pathways in a meaningful manner. Clinical trials of novel agents impacting these pathways have demonstrated efficacy and improved outcomes in asthma exacerbations, control, and forced expiratory volume in 1 second (FEV1) in patients with severe asthma. Future treatments in asthma will focus on drugs that target these aforementioned cytokines.
Keywords: antibody; exacerbations; forced expiratory volume in 1 second (fev1); ige; respiratory biologics; severe asthma; t-helper cells.
Copyright © 2019, Johnson et al.