[Cigarette smoke-induced acute airway impairment].
Cigarette smoking has been implicated in many pulmonary disorders, including chronic bronchitis and chronic obstructive lung disease. Cigarette smoking is associated with increased airway responsiveness. Acute exposure to cigarette smoke increases airway responsiveness in a dose-dependent manner. A superoxide is involved in airway hyper-responsiveness induced by cigarette smoke, perhaps by direct toxic action. Cigarette smokers have increased numbers of neutrophils present in their lower respiratory tract. Acute exposure to cigarette smoke initiates a superoxide-dependent mechanism that, through NF-kappa B activation and IL-8 expression, induces infiltration of neutrophils into the airways in vivo. The alveolar macrophage is one potential source of NF-kappa B activation and IL-8 production after acute exposure to cigarette smoke. Manipulation of NF-kappa B by antioxidants in vivo may be useful in limiting biologic processes such as pro-inflammatory cytokine production, which may lead to neutrophil accumulation in the lung.
Nishikawa
M
M
Department of Respiratory Medicine, Fujisawa City Hospital.
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D016535:Bronchial Hyperreactivity / Q000209:etiology*; D001991:Bronchitis / Q000209:etiology; D006801:Humans; D016209:Interleukin-8 / Q000378:metabolism; D008173:Lung Diseases, Obstructive / Q000209:etiology*; D016676:Macrophages, Alveolar / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D020556:Neutrophil Infiltration / Q000187:drug effects; D012137:Respiratory System / Q000166:cytology; D012907:Smoking / Q000009:adverse effects*; D013481:Superoxides
D000975:Antioxidants; D016209:Interleukin-8; D016328:NF-kappa B; D013481:Superoxides