title: Airway inflammation and remodeling in asthma.
abstract: An important advance in our understanding of the pathophysiology of asthma has been the discovery that airway inflammation is not confined to severe asthma but also characterizes mild and moderate asthma. Inflammation in asthma may be the result of a peculiar type of lymphocytic inflammation whereby Th2 lymphocytes secrete cytokines that orchestrate cellular inflammation and promote airway hyperresponsiveness. The term "airway remodeling" in asthma refers to structural changes that occur in conjunction with, or because of, chronic airway inflammation. Airway remodeling results in alterations in the airway epithelium, lamina propria, and submucosa, leading to thickening of the airway wall. The consequences of airway remodeling in asthma may include incompletely reversible airway narrowing, bronchial hyperresponsivenesss, airway edema, and mucus hypersecretion. Airway remodeling in asthma thus may predispose persons with asthma to asthma exacerbations and even death from airway obstruction caused by smooth muscle contraction, airway edema, and mucus plugging. Although much has been learned in the past 25 years about the pathophysiology of airway inflammation and airway remodeling in asthma, important questions remain about the relation between airway inflammation and remodeling, the natural history of airway remodeling, and the effects of current asthma treatments on remodeled airways.
authors.affiliation: Department of Medicine and the Cardiovascular Research Institute, University of California at San Francisco, 94143-0111, USA.
authors.forename: J V
authors.initials: JV
authors.lastname: Fahy
authors.forename: D B
authors.initials: DB
authors.lastname: Corry
authors.forename: H A
authors.initials: HA
authors.lastname: Boushey
mesh_terms: D000402:Airway Obstruction / Q000503:physiopathology; D001249:Asthma / Q000473:pathology / Q000503:physiopathology*; D001485:Basement Membrane / Q000473:pathology / Q000503:physiopathology; D001980:Bronchi / Q000473:pathology / Q000503:physiopathology*; D016535:Bronchial Hyperreactivity / Q000503:physiopathology; D001991:Bronchitis / Q000473:pathology / Q000503:physiopathology*; D003251:Constriction, Pathologic / Q000473:pathology; D016207:Cytokines / Q000502:physiology; D004487:Edema / Q000473:pathology; D004848:Epithelium / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D009093:Mucus / Q000378:metabolism; D009119:Muscle Contraction / Q000502:physiology; D009130:Muscle, Smooth / Q000503:physiopathology; D020545:Respiratory Mucosa / Q000473:pathology / Q000503:physiopathology; D012307:Risk Factors; D013224:Status Asthmaticus / Q000503:physiopathology; D018418:Th2 Cells / Q000502:physiology
chemical_list: D016207:Cytokines