Epithelial dysfunction and airway hyperreactivity in asthma.
It is clear that the central airway epithelium plays an important role in restricting access of inhaled solutes to sub-epithelial airway wall structures. Non-specific airway hyperreactivity to spasmogens in asthma may result partly as a consequence of the compromise of the epithelium as a barrier to solute diffusion. However, impaired epithelial production and release of smooth muscle relaxant factor(s) may also contribute to airway hyperresponsiveness. Virally precipitated asthma also involves inflammation-induced epithelial damage. Beta-adrenoceptor hypofunction induced by respiratory viruses may also contribute to bronchial obstruction.
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001249:Asthma / Q000209:etiology / Q000503:physiopathology*; D001685:Biological Factors; D001980:Bronchi / Q000503:physiopathology*; D001986:Bronchial Spasm / Q000209:etiology / Q000503:physiopathology*; D004848:Epithelium / Q000378:metabolism; D006801:Humans; D009124:Muscle Proteins / Q000502:physiology; D009130:Muscle, Smooth / Q000503:physiopathology*; D009569:Nitric Oxide; D011453:Prostaglandins / Q000502:physiology*; D012141:Respiratory Tract Infections / Q000503:physiopathology; D014777:Virus Diseases / Q000503:physiopathology
D000319:Adrenergic beta-Antagonists; D001685:Biological Factors; D009124:Muscle Proteins; D011453:Prostaglandins; C056250:epithelium-derived relaxant factor; D009569:Nitric Oxide