Analysis of IL-6 mRNA expression in BALF cells from IPF patients

IPF患者BALF细胞IL-6 mRNA表达分析

• 批准号: 04670466
• 负责人: HAYASHI Seiji
• 金额: $ 1.28万
• 依托单位: Osaka- University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1992
• 资助国家: 日本
• 起止时间: 1992 至 1993
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-04670466/
• 关键词: RT-PCR; IPF; IL-6; BAL; 特発性間質性肺炎; 気管支肺胞洗浄細胞; サイトカイン; 増殖因子

The pathogenesis of fibrosing lung disease likely involves inflammatory cytokines secreted from immune effector cells. In this study RNAs were extracted from bronchoalveolar lavage fluid (BALF) cells obtained from patients with idiopathic interstitial pneumonia (IIP) (n=9), asbestosis (n=4), silicosis (n=8), lung cancer( n=6) and healthy volunteers(n=12), and mRNAs for cytokines were assessed by amplofication with reverse transcription-polymerase chain reaction(RT-PCR). The quantitative results were expressed as ratios of the amount of PCR products of cytokines and beta-actin as an internal control. The expression of TGF-beta mRNA was elevated jin the patients with IIP, asbestosis and silicosis as compared with controls of the lung cancer patients and the healthy volunteers. The expressions of IL-1beta and TNFalpha mRNA in BALF cells and IL-1beta protein titer in BALF were both suppressed in the patients with these three diseases. No significant differences were observed in the expression of IL-8 or IL-6 mRNA between the patients with lung fibrosis and the healthy volunteers. Prostaglandin E2 (PGE2) concentration in BALF from patients with lung fibrosis was higher as compared to healthy volunteers. The decreases in IL-1beta and TNFalpha production may be, in part, due to high level of PGE2 in BALF from patients. These results suggest that regulatory mechanism (s) of IL-1beta, TNFalpha and TGF-beta may be common to patients with IIP, asbestosis and silicosis, and these cytokines may significantly contribute to the alveolar damage and subseqent fibrosis. To characterriza the biololgical roles of cytokines and growth-factors in vivo, we are planning to introduce TGFbeta gene into rat lung by using HVJ-liposome.

纤维化肺病的发病机制可能涉及免疫效应细胞分泌的炎症细胞因子。本研究从特发性间质性肺炎 (IIP) (n=9)、石棉肺 (n=4)、矽肺 (n=8)、肺癌 (n=6) 和健康志愿者 (n=12) 患者的支气管肺泡灌洗液 (BALF) 细胞中提取 RNA，并通过反向扩增来评估细胞因子的 mRNA。 转录聚合酶链反应（RT-PCR）。定量结果表示为细胞因子和作为内参的β-肌动蛋白的PCR产物量的比率。与肺癌患者和健康志愿者的对照相比，IIP、石棉肺和矽肺患者的 TGF-β mRNA 表达升高。这三种疾病患者BALF细胞中IL-1β和TNFα mRNA的表达以及BALF中IL-1β蛋白滴度均受到抑制。肺纤维化患者与健康志愿者之间IL-8或IL-6 mRNA的表达没有观察到显着差异。肺纤维化患者 BALF 中的前列腺素 E2 (PGE2) 浓度高于健康志愿者。 IL-1β 和 TNFα 产生的减少可能部分是由于患者 BALF 中 PGE2 水平较高。这些结果表明，IL-1β、TNFα和TGF-β的调节机制对于IIP、石棉肺和矽肺患者可能是常见的，并且这些细胞因子可能显着促进肺泡损伤和随后的纤维化。为了表征细胞因子和生长因子在体内的生物学作用，我们计划使用 HVJ 脂质体将 TGFbeta 基因导入大鼠肺中。

项目成果

Isao Tachibana et al: "Generation of a small cell lung cancer variant resistant to lymphokine-activated killer(LAK)cells." Cancer Research. 52. 3310-3316 (1992)

Isao Tachibana 等人：“产生对淋巴因子激活杀伤 (LAK) 细胞具有抗性的小细胞肺癌变体。”

Isao Tachibana, Masatoshi Watanabe, Yoshiro Tanio, Seiji Hayashi, Shinich Saito, Machiko Matsunashi, Tadashi Osaki, Yohsihisa Shigedeo, Tomiya Masuno, and Ichiro Kawase: "Generation of a small cell lung cancer variant resistant to lymphokine-activated kil

Isao Tachibana、Masatoshi Watanabe、Yoshiro Tanio、Seiji Hayashi、Shinich Saito、Machiko Matsunashi、Tadashi Osaki、Yohsihisa Shigedeo、Tomiya Masuno 和 Ichiro Kawase：“产生对淋巴因子激活 kil 具有抗性的小细胞肺癌变体

佐久間順子 他: "放射線照射による気管支肺胞洗浄細胞組成の変化の検討" 気管支学. 15. 823-824 (1993)

Junko Sakuma 等人：“辐射照射引起的支气管肺泡灌洗细胞成分变化的检查”《支气管学》15. 823-824 (1993)。

Isao Tachibana et al: "Generation of a small cell lung cancer variant resistant to lymphokine-activated killer(LAK)cells:Association with resistance to a LAK cell-derived,cytotoxic factor" Cancer Research. 52. 3310-3316 (1992)

Isao Tachibana 等人：“抗淋巴因子激活杀伤 (LAK) 细胞的小细胞肺癌变体的产生：与对 LAK 细胞衍生的细胞毒性因子抗性的关联”癌症研究。

佐久間 順子 他: "放射線照射による気管支肺胞洗浄細胞組成の変化の検討" 気管支学. 15. 823-824 (1993)

Junko Sakuma 等人：“辐射照射引起的支气管肺泡灌洗细胞成分变化的检查”《支气管学》15. 823-824 (1993)。