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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >The IL-4Ralpha pathway in macrophages and its potential role in silica-induced pulmonary fibrosis.
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The IL-4Ralpha pathway in macrophages and its potential role in silica-induced pulmonary fibrosis.

机译：巨噬细胞中的IL-4Ralpha途径及其在二氧化硅诱导的肺纤维化中的潜在作用。

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Crystalline silica exposure can result in pulmonary fibrosis, where the pulmonary macrophage is key as a result of its ability to react to silica particles. In the mouse silicosis model, there is initial Th1-type inflammation, characterized by TNF-alpha and IFN-gamma. Previous studies determined that Th2 mediators (i.e., IL-13) are vital to development of pulmonary fibrosis. The present study, using in vivo and in vitro techniques, compares silica exposures between Balb/c and Th2-deficient mice in an effort to determine the link between Th2 immunity and silicosis. In long-term experiments, a significant increase in fibrosis and activated interstitial macrophages was observed in Balb/c but not IL-4Ralpha(-/-) mice. Additionally, a significant increase in Ym1 mRNA levels, a promoter of Th2 immunity, was determined in the interstitial leukocyte population of silica-exposed Balb/c mice. To elucidate the effects of silica on macrophage function, bone marrow-derived macrophages (BMdM) were exposed to particles and assayed for T cell (TC) stimulation activity. As a control, Ym1 mRNA expression in Balb/c BMdM was determined using IL-4 stimulation. In the in vitro assay, a significant increase in TC activation, as defined by surface markers and cytokines, was observed in the cultures containing the silica-exposed macrophages in wild-type and IL-4Ralpha(-/-) mice, with one exception: IL-4Ralpha(-/-) BMdM were unable to induce an increase in IL-13. These results suggest that crystalline silica alters cellular functions of macrophages, including activation of TC, and that the increase in Th2 immunity associated with silicosis is via the IL-4Ralpha-Ym1 pathway.
机译：结晶性二氧化硅暴露会导致肺纤维化，其中肺巨噬细胞由于其与二氧化硅颗粒反应的能力而成为关键。在小鼠矽肺病模型中，最初存在Th1型炎症，其特征是TNF-α和IFN-γ。先前的研究确定Th2介质（即IL-13）对肺纤维化的发展至关重要。本研究使用体内和体外技术，比较了Balb / c和Th2缺陷型小鼠之间的二氧化硅暴露量，目的是确定Th2免疫力和矽肺病之间的联系。在长期实验中，在Balb / c小鼠中观察到纤维化和激活的间质巨噬细胞显着增加，但在IL-4Ralpha（-/-）小鼠中未观察到。此外，在暴露于二氧化硅的Balb / c小鼠的间质白细胞群体中，确定了Th2免疫的启动子Ym1 mRNA水平显着增加。为了阐明二氧化硅对巨噬细胞功能的影响，将骨髓衍生的巨噬细胞（BMdM）暴露于颗粒中并测定T细胞（TC）刺激活性。作为对照，使用IL-4刺激测定Balb / c BMdM中Ym1 mRNA的表达。在体外测定中，在野生型和IL-4Ralpha（-/-）小鼠中，在含有二氧化硅暴露的巨噬细胞的培养物中，观察到了由表面标志物和细胞因子定义的TC活化的显着增加，只有一个例外：IL-4Ralpha（-/-）BMdM无法诱导IL-13的增加。这些结果表明，结晶二氧化硅会改变巨噬细胞的细胞功能，包括TC的激活，并且与矽肺病相关的Th2免疫力的提高是通过IL-4Ralpha-Ym1途径实现的。

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