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哮喘和 COPD 中炎症机制的差异。

Differences of inflammatory mechanisms in asthma and COPD.

机构信息

Third Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan.

出版信息

Allergol Int. 2009 Sep;58(3):307-13. doi: 10.2332/allergolint.09-RAI-0106. Epub 2009 Jul 25.

DOI:10.2332/allergolint.09-RAI-0106
PMID:19628975
Abstract

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.

摘要

支气管哮喘和慢性阻塞性肺疾病(COPD)是日益常见的疾病。这两种疾病的主要发病机制是慢性炎症。然而,每种疾病的炎症模式是不同的。在哮喘气道中,活化的肥大细胞/嗜酸性粒细胞和辅助性 T 淋巴细胞 2(Th2)占优势。相比之下,巨噬细胞和中性粒细胞在 COPD 气道/肺中很重要。虽然在哮喘和 COPD 中观察到诱导型一氧化氮合酶(iNOS)导致的一氧化氮(NO)过度产生,但通过 NO 与 O(2)之间的反应形成的硝基酪氨酸以及髓过氧化物酶介导的途径。这两种疾病中不同的炎症模式似乎导致了哮喘和 COPD 的病理差异。

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