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首页> 外文期刊>Archives of Toxicology >IL-6 receptor-mediated lung Th2 cytokine networking in silica-induced pulmonary fibrosis
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IL-6 receptor-mediated lung Th2 cytokine networking in silica-induced pulmonary fibrosis

机译：IL-6受体介导的肺Th2细胞因子网络在二氧化硅诱导的肺纤维化中的作用

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Pulmonary silicosis is a deadly disease which kills thousands of people every year worldwide. The disease initially develops as an inflammatory response with recruitment of inflammatory cells into the lung controlled by multiple cytokines. The question whether these cytokines exert biological functions through signal transducing pathway remains unanswered along with the potential role of interleukin-6 receptor α (IL-6Rα) in regulating inflammatory cytokines. We aimed to assess the status of signal transducers and activator of transcription (Stat3), suppressor of cytokine signalling 3(Socs3) and inflammatory cytokines in airways of silica-exposed mice, and their relationship with IL-6Rα. Silica-exposed and silica-exposed IL-6Rα gene knockdown Balb/c mice were used in the study. Lung function was measured by plethysmography, mRNA expression of cytokines and signal molecules by qRT2-PCR and lung architecture by histopathology; T helper cell-type 2 (Th2) cytokines in broncho-alveolar lavage fluids were evaluated by ELISA and hydroxyproline in lung by colorimetry. Elevated levels of collagen deposition, signs of lung fibrosis, infiltration of inflammatory cells and presence of exfoliated mucosa in the lung of silica-exposed mice with concurrent increase in methacholine-induced specific resistance of airways were observed on day 60 post-exposure. In parallel, heightened expression of Th2 cytokines (IL-4, IL-5, IL-6) and signal molecules (Stat3 and Socs3) were observed in the airways of silica-exposed mice. Th1 (IL-1β and TNF-α) cytokines are underexpressed in majority of the airways tissues of silica-exposed mice. Silencing IL-6Rα in lung of silica-exposed mice down regulated the hypermorphic mRNA pool of potential Th2 cytokines and signal molecules. Hypermorphic expression of Th2 cytokines and signal molecules in airways of silica-exposed mice are mediated through IL-6Rα.
机译：肺矽肺病是一种致命的疾病，全世界每年有数千人丧生。该疾病最初发展为炎症反应，炎症细胞被多种细胞因子控制进入肺部。这些细胞因子是否通过信号转导途径发挥生物学功能，以及白介素6受体α（IL-6Rα）在调节炎症细胞因子方面的潜在作用仍未得到解答。我们旨在评估暴露于二氧化硅的小鼠气道中信号转导和转录激活子（Stat3），细胞因子信号传导抑制剂3（Socs3）和炎性细胞因子的抑制状态，以及它们与IL-6Rα的关系。暴露于二氧化硅和暴露于二氧化硅的IL-6Rα基因敲除Balb / c小鼠用于研究。体积描记法检测肺功能，qRT 2 -PCR检测细胞因子和信号分子的mRNA表达，组织病理学检测肺结构。 ELISA法检测支气管肺泡灌洗液中的T辅助细胞2型（Th2）细胞因子，比色法检测肺中的羟脯氨酸。暴露后第60天，观察到二氧化硅暴露的小鼠肺中胶原蛋白沉积水平升高，肺纤维化的体征，炎性细胞浸润和肺剥落黏膜的存在，同时乙酰甲胆碱诱导的气道比抵抗同时增加。同时，在暴露于二氧化硅的小鼠的气道中观察到Th2细胞因子（IL-4，IL-5，IL-6）和信号分子（Stat3和Socs3）的表达增加。 Th1（IL-1β和TNF-α）细胞因子在二氧化硅暴露的小鼠的大多数气道组织中表达不足。二氧化硅暴露小鼠肺中沉默的IL-6Rα会下调潜在的Th2细胞因子和信号分子的高形态mRNA池。暴露于二氧化硅的小鼠气道中Th2细胞因子和信号分子的过高表达是通过IL-6Rα介导的。

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