The role of IL-13 gene polymorphism in the exacerbation of Asthma severity

Abstract

Asthma is a chronic airway inflammatory disorder characterized by persistent inflammation, obstruction, and hyperresponsiveness. The role of cytokines, particularly Interleukin-13 (IL-13), in the pathogenesis of asthma has been extensively studied. IL-13 is involved in Th2 inflammation and has been identified as a possible therapeutic target in asthma treatment. This review focuses on the role of IL-13 gene polymorphism in exacerbating asthma severity. IL-13 is responsible for various key pathological features of asthma, including airway hyper- responsiveness, mucus production, and induction of allergic responses. The release of IL-13 is triggered by exposure to allergens, which activate dendritic cells and promote the differentiation of Th2 cells. IL-13 interacts with its receptors, IL-13Rá1 and IL-13Rá2, and initiates signaling pathways involving JAK1, JAK3, and STAT6. Biomarkers such as total serum IgE, exhaled nitric oxide (FeNO), airway epithelial proteins, blood eosinophil counts, and sputum eosinophil counts have been used to assess IL-13 activity and predict treatment response. Polymorphisms in the IL-13 gene and its receptors have been associated with asthma susceptibility, severity, and response to therapy. Understanding the role of IL-13 gene and polymorphism in asthma can provide insights into disease mechanisms and contribute to personalized treatment approaches. Further studies are needed to elucidate the association airway between IL-13 polymorphisms, asthma severity, and response to inhaled corticosteroids (ICS).