Differences of inflammatory mechanisms in asthma and COPD.
Bronchial asthma and chronic obstructive pulmonary disease (COPD) are increasing common diseases. The major pathogenesis of both illnesses is chronic inflammation. However, the inflammatory pattern is distinct in each disease. In asthmatic airways, activated mast cells/eosinophils and T helper 2 lymphocytes (Th2) are predominant. In contrast, macrophages and neutrophils are important in COPD airways/lung. Although nitric oxide (NO) hyperproduction due to inducible NO synthase (iNOS) is observed in asthma and COPD, nitrotyrosine formation via the reaction between NO and O(2)- in addition to the myeloperoxidase-mediated pathway. These distinct inflammatory patterns in both diseases seem to cause pathological differences in asthma and COPD.
Ichinose
Masakazu
M
Third Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan. masakazu@wakayama-med.ac.jp
D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000378:metabolism; D004804:Eosinophils / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000276:immunology* / Q000378:metabolism; D008168:Lung / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D009504:Neutrophils / Q000276:immunology; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D029424:Pulmonary Disease, Chronic Obstructive / Q000276:immunology* / Q000378:metabolism; D018418:Th2 Cells / Q000276:immunology
D009569:Nitric Oxide; D009195:Peroxidase; D052247:Nitric Oxide Synthase Type II; D010100:Oxygen