巨噬细胞向肌成纤维细胞转化对矽肺病的影响。

Q1 Health Professions
Fei Geng, Jingrou Xu, Xichen Ren, Ying Zhao, Yuhao Cai, Yaqian Li, Fuyu Jin, Tian Li, Xuemin Gao, Wenchen Cai, Hong Xu, Zhongqiu Wei, Na Mao, Ying Sun, Fang Yang
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引用次数: 0

摘要

背景:目的是探讨巨噬细胞极化和巨噬细胞向肌成纤维细胞转化(MMT)对矽肺的影响:目的:探讨巨噬细胞极化和巨噬细胞向肌成纤维细胞转化(MMT)对矽肺的影响:雄性 Wistar 大鼠分为对照组和使用 HOPE MED 8050 动态自动除尘系统开发的矽肺组。将小鼠巨噬细胞 MH-S 随机分为对照组和二氧化硅组。使用苏木精、伊红(HE)和范吉森(VG)染色法观察肺组织的病理变化。采用免疫组化和免疫荧光染色法检测巨噬细胞标记物(F4/80)、M1巨噬细胞标记物(iNOS)、M2巨噬细胞标记物(CD206)和肌成纤维细胞标记物(α-平滑肌肌动蛋白[α-SMA])的分布和位置。采用 Western 印迹法测定 iNOS、Arg、α-SMA、波形蛋白和 I 型胶原(Col I)的表达变化:结果:HE和VG染色结果显示,矽肺组肺组织中有明显的硅结节形成和粗胶原纤维分布。巨噬细胞标记物F4/80在接触二氧化硅后8周至32周逐渐增加。免疫组化和免疫荧光染色结果显示,8周时,矽肺组的肺组织中有更多的iNOS阳性细胞和一些CD206阳性细胞。32 周时,在矽肺组肺组织的硅结节中发现了更多的 CD206 阳性细胞。Western blot 分析显示,与对照组相比,矽肺组肺组织中诱导型一氧化氮合酶和 Arg 蛋白的表达上调。免疫荧光染色结果显示,F4/80、α-SMA和Col I在矽肺组肺组织中同时表达,CD206和α-SMA在矽肺组肺组织中同时表达。用免疫荧光染色法检测大鼠肺泡灌洗液,发现F4/80+α-SMA+、CD206+α-SMA+和F4/80+α-SMA+Col I+细胞。在二氧化硅诱导的 MH-S 细胞中也发现了类似的结果:结论:矽肺的发展伴随着巨噬细胞极化和MMT。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of macrophage-to-myofibroblast transition on silicosis.

Background: The aim was to explore the effect of macrophage polarization and macrophage-to-myofibroblast transition (MMT) in silicosis.

Methods: Male Wistar rats were divided into a control group and a silicosis group developed using a HOPE MED 8050 dynamic automatic dusting system. Murine macrophage MH-S cells were randomly divided into a control group and an SiO2 group. The pathological changes in lung tissue were observed using hematoxylin and eosin (HE) and Van Gieson (VG) staining. The distribution and location of macrophage marker (F4/80), M1 macrophage marker (iNOS), M2 macrophage marker (CD206), and myofibroblast marker (α-smooth muscle actin [α-SMA]) were detected using immunohistochemical and immunofluorescent staining. The expression changes in iNOS, Arg, α-SMA, vimentin, and type I collagen (Col I) were measured using Western blot.

Results: The results of HE and VG staining showed obvious silicon nodule formation and the distribution of thick collagen fibers in the lung tissue of the silicosis group. Macrophage marker F4/80 increased gradually from 8 to 32 weeks after exposure to silica. Immunohistochemical and immunofluorescent staining results revealed that there were more iNOS-positive cells and some CD206-positive cells in the lung tissue of the silicosis group at 8 weeks. More CD206-positive cells were found in the silicon nodules of the lung tissues in the silicosis group at 32 weeks. Western blot analysis showed that the expressions of Inducible nitric oxide synthase and Arg protein in the lung tissues of the silicosis group were upregulated compared with those of the control group. The results of immunofluorescence staining showed the co-expression of F4/80, α-SMA, and Col I, and CD206 and α-SMA were co-expressed in the lung tissue of the silicosis group. The extracted rat alveolar lavage fluid revealed F4/80+α-SMA+, CD206+α-SMA+, and F4/80+α-SMA+Col I+ cells using immunofluorescence staining. Similar results were also found in MH-S cells induced by SiO2.

Conclusions: The development of silicosis is accompanied by macrophage polarization and MMT.

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