PATHOPHYSIOLOGY OF ASTHMA: A REVIEW

This review aims to provide a brief overview of different mechanisms involved in the pathophysiology of asthma, a variety of cells, and mediators released from these cells, which have an important role in the pathophysiology of asthma. Asthma is a heterogeneous disease which having complex pathophysiology and affects many individuals. Asthma is an inflammatory disease in the airway, leading to airway hyperresponsiveness, obstruction, mucus hyper-production, and airway wall remodeling. Status asthmatics is characterized by hypoxemia, hypercarbia, and secondary respiratory failure. The structural, mechanical, and inflammatory abnormalities related to asthma and the different mediators like histamine, cytokines, leukotrienes, thromboxane’s inflammatory cells eosinophils, mast cells are important in asthma pathophysiology. TGF-h and IL-11 are the main cytokines that are involved in airway remodeling. Mast cells are responsible for initiating inflammatory responses after exposure to allergens and the resulting immediate bronchoconstriction. Macrophages releasing the mediators may be responsible for amplifying the inflammatory process. Dendritic cells act as antigen-presenting cells and play a role in the chemotaxis of T cells. Eosinophils are a source of lipid-derived mediators (leukotrienes), and eosinophil granules contain major basic protein (MBP), eosinophil cationic factor (ECF), eosinophil-derived neurotoxin and eosinophil-peroxidase. These may be responsible for respiratory tract fibrinogenesis and airway hyperresponsiveness. Adenosine causes bronchoconstriction in asthmatics but not in non-asthmatics. Toll-like receptors serve as receptors for products generated by pathogens. The etiology of asthma is increasingly associated with interactions between genetic susceptibility, host factors, and environmental exposures.