Lakari Essi, Soini Ylermi, Säily Marjaana, Koistinen Pirjo, Pääkkö Paavo, Kinnula Vuokko L
Department of Internal Medicine, University of Oulu and Oulu University Hospital, Finland.
Am J Clin Pathol. 2002 Jan;117(1):132-42. doi: 10.1309/w7t9-hw9v-v94b-r9km.
We assessed the distribution and expression of inducible nitric oxide synthase (i-NOS), endothelial nitric oxide synthase (e-NOS), and xanthine oxidase (XAO) in usual interstitial pneumonia, desquamative interstitial pneumonia, and granulomatous diseases. The material consisted of biopsy specimens from 5 healthy subjects (nonsmokers), 9 patients with usual interstitial pneumonia, 11 with desquamative interstitial pneumonia, 14 with sarcoidosis, and 8 with extrinsic allergic alveolitis. i-NOS was expressed intensively in inflammatory but not infibrotic lesions. It was expressed most prominently in alveolar macrophages and alveolar epithelium of all disorders and in the granulomas of sarcoidosis and extrinsic allergic alveolitis. In contrast with i-NOS, e-NOS was expressed prominently in control lung tissue samples but also in granulomas of sarcoidosis and extrinsic allergic alveolitis. Reverse transcription-polymerase chain reaction performed on bronchoalveolar lavage fluid samples from patients with sarcoidosis or usual interstitial pneumonia andfrom healthy subjects indicated positivity for XAO, but immunohistochemical analysis in samples from healthy lung and all parenchymal lung disorders showed no immunoreactivity for XAO. i-NOS has an important role in the pathogenesis of interstitial lung diseases, being up-regulated during the inflammatory but not during the fibrotic disease stage.
我们评估了诱导型一氧化氮合酶(i-NOS)、内皮型一氧化氮合酶(e-NOS)和黄嘌呤氧化酶(XAO)在寻常型间质性肺炎、脱屑性间质性肺炎和肉芽肿性疾病中的分布及表达情况。材料包括来自5名健康受试者(非吸烟者)、9例寻常型间质性肺炎患者、11例脱屑性间质性肺炎患者、14例结节病患者和8例外源性过敏性肺泡炎患者的活检标本。i-NOS在炎症性而非纤维化性病变中表达强烈。在所有疾病的肺泡巨噬细胞和肺泡上皮中以及结节病和外源性过敏性肺泡炎的肉芽肿中,其表达最为显著。与i-NOS相反,e-NOS在对照肺组织样本中表达显著,在结节病和外源性过敏性肺泡炎的肉芽肿中也有表达。对结节病或寻常型间质性肺炎患者以及健康受试者的支气管肺泡灌洗液样本进行逆转录聚合酶链反应显示XAO呈阳性,但对健康肺组织和所有实质性肺疾病样本的免疫组织化学分析显示XAO无免疫反应性。i-NOS在间质性肺疾病的发病机制中起重要作用,在炎症性疾病阶段而非纤维化疾病阶段上调。