A study of interstitial pneumonia with HCV transgenic mouse

HCV转基因小鼠间质性肺炎的研究

• 批准号: 11670592
• 负责人: NAKANO Junici
• 金额: $ 1.86万
• 依托单位: Teikyo University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1999
• 资助国家: 日本
• 起止时间: 1999 至 2000
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11670592/
• 关键词: pulmonary fibrosis; mouse; hepatitis C virus; transgenic; cytokine; silica; PDGF; interstitial pneumonia; C型肝炎ウイルス; PDGF; トランスジェニックマウス; 特発性間質性肺炎; core protein; envelope protein; シェーグレン症候群; 肉芽腫

Pathogenesis of IIP (idiopathic interstitial pneumonia) is still unclear despite of its poor prognosis. We hypothesized that HCV (hepatitis C virus), which has been recognized as one of major pathogen of fibrous change in liver, may play a role in IIP.First, we confirmed significantly high population of patients with IIP have antibody against HCV and patients with IIP are more frequently positive in RT-PCR to HCV as compared to controls. In this study we investigated the role of this virus in IIP with HCV transgenic mouse by our murine model for IIP.HCV transgenic mouse has significantly more lymphocytes in BALF as compared to wild type mouse in natural course. Furthermore, at the point of 2 weeks after silica particulate instillation, HCV transgenic mouse had much more doses of hydroxyproline (wild : wild+silica : HCVenv : HCVenv+silica = 150±45 : 350±32 : 295±40 : 438±48) and higher pathological scores for IIP as compared to those of wild type mouse with same treatment. These findings proposed that HCV might promote the progression of fibrous changes in lung in response to silica.

特发性间质性肺炎（IIP）的发病机制尚不清楚，尽管其预后不良。我们假设，HCV（丙型肝炎病毒），这已被公认为是一个主要的病原体在肝脏纤维化的变化，可能会在IIP中发挥作用。首先，我们证实了显着高人口的IIP患者有抗HCV抗体和IIP患者更频繁地在RT-PCR阳性HCV相比，对照组。本研究通过建立HCV转基因小鼠IIP模型，研究了HCV在IIP中的作用。此外，在二氧化硅颗粒滴注后2周的时间点，HCV转基因小鼠与具有相同处理的野生型小鼠相比具有更多剂量的羟脯氨酸（野生型：野生型+二氧化硅：HCVenv：HCVenv+二氧化硅= 150 ± 45：350 ± 32：295 ± 40：438 ± 48）和更高的IIP病理评分。这些结果表明，HCV可能会促进响应二氧化硅的肺纤维化的进展。