Inflammatory mechanisms and nocturnal asthma.
The results of recent research strongly suggest that airway inflammation, which may increase at night as a result of circadian troughs in blood epinephrine and cortisol concentrations, underlies the bronchial hyperresponsiveness that is almost certainly a major contributor to the pathogenesis of nocturnal asthma. This article reviews what is known about the nature and complex interactions of the inflammatory cells and mediators that may be involved in asthma, with particular emphasis on nocturnal asthma. The roles of platelet-activating factor antagonists, corticosteroids, and theophylline in suppressing this response also are discussed.
D000241:Adenosine / Q000502:physiology; D001249:Asthma / Q000503:physiopathology*; D001792:Blood Platelets / Q000502:physiology; D002940:Circadian Rhythm; D004804:Eosinophils / Q000502:physiology; D004848:Epithelium / Q000502:physiology; D006632:Histamine / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D008214:Lymphocytes / Q000502:physiology; D008264:Macrophages / Q000502:physiology; D008407:Mast Cells / Q000502:physiology; D009504:Neutrophils / Q000502:physiology; D010972:Platelet Activating Factor / Q000502:physiology; D011453:Prostaglandins / Q000502:physiology; D013189:SRS-A / Q000502:physiology
D010972:Platelet Activating Factor; D011453:Prostaglandins; D013189:SRS-A; D006632:Histamine; D000241:Adenosine