Asthma: Pathogenesis, Etiology, and Risk Factors

Abstract

Asthma is a chronic respiratory disorder characterized by chronic inflammation and airway hyperresponsiveness, causing symptoms such as breathlessness, coughing, wheezing, and dyspnea. It is defined as a complex hereditary disease with marginal influences from numerous genetic variables that react with numerous environmental agents to modify disease severity and susceptibility. With T helper 2 (Th2) lymphocytes, mast cells, immunoglobulin E (IgE), macrophages, eosinophils, and cytokines, the illness is more complex than a simple allergic reaction. Additionally, it involves local mesenchymal, vascular, neurologic, and epithelial processes that drive the Th2 phenotype to the lungs and result in aberrant injury–repair mechanisms that remodel the airway wall. The pathophysiology processes of asthma are significantly influenced by cytokines; thus, it is imperative to comprehend the composition, regulation, and mutations of the genes encoding these molecules.