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Exposure to a combination of silica nanoparticles and low-dose radiation aggravates lung fibrosis in mice via gut microbiota modulation
Environmental Science: Nano ( IF 5.8 ) Pub Date : 2020-11-16 , DOI: 10.1039/d0en01021a Zhao Ju 1, 2, 3, 4, 5 , Guofeng Ren 2, 3, 4, 5 , Meiling Zhou 1, 2, 3, 4, 5 , Jin Jing 1, 2, 3, 4, 5 , Jing Xiang 1, 2, 3, 4, 5 , Xiaodan Liu 6, 7, 8, 9, 10 , Ruixue Huang 1, 2, 3, 4, 5 , Ping-Kun Zhou 6, 7, 8, 9, 10
Environmental Science: Nano ( IF 5.8 ) Pub Date : 2020-11-16 , DOI: 10.1039/d0en01021a Zhao Ju 1, 2, 3, 4, 5 , Guofeng Ren 2, 3, 4, 5 , Meiling Zhou 1, 2, 3, 4, 5 , Jin Jing 1, 2, 3, 4, 5 , Jing Xiang 1, 2, 3, 4, 5 , Xiaodan Liu 6, 7, 8, 9, 10 , Ruixue Huang 1, 2, 3, 4, 5 , Ping-Kun Zhou 6, 7, 8, 9, 10
Affiliation
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Exposure to silica nanoparticles (SNPs) causes lung fibrosis and threatens human health. However, it is unknown if low-dose radiation (LDR) exposure exacerbates SNP-induced lung dysfunction. Thus, the aim of our study was to determine the combined effect of SNPs and LDR on lung fibrosis and elucidate the potential mechanisms involved. We used SNP-induced A549 cells and mouse models and detected gut microbiota alteration by 16S rDNA amplicon sequencing. Additionally, lung fibrosis-related parameters were also detected using hematoxylin and eosin (H&E) staining, immunofluorescence (IF) staining, qRT-PCR, and western blot analysis. The histopathological and IF staining assays illustrated that co-exposure of mice to SNPs and LDR had a significant deleterious effect on both lung function and lung fibrosis, in comparison to exposure to SNPs or LDR alone. Furthermore, the abundance of Bacteroidetes significantly increased while that of Firmicutes significantly decreased following co-exposure to SNPs and LDR. Mechanistically, the Notch cascade was activated in chronically SNP-exposed mice with lung fibrosis and A549 cells. Additionally, the Notch pathway-associated proteins showed increased expression levels in the lungs following SNP exposure both in vivo and in vitro. Notably, SNP-induced dysbiosis of the gut microbiota promoted lung epithelial damage by triggering the Notch pathway, resulting in SNP-induced lung fibrosis. However, oral administration of probiotics protected the mice from SNP-induced lung injury. Our results strongly indicate that the activation of the gut microbiota-dependent Notch pathway in response to co-exposure to SNPs and LDR results in lung epithelial injury in vivo. Probiotics supplementation is a potential way to protect against SNP- and LDR-induced lung fibrosis.
中文翻译：
暴露于二氧化硅纳米颗粒和低剂量辐射的组合会通过肠道微生物群调节加重小鼠肺纤维化
暴露于二氧化硅纳米颗粒（SNP）会导致肺纤维化并威胁人体健康。然而，尚不清楚低剂量辐射（LDR）暴露是否会加剧SNP诱导的肺功能障碍。因此，我们研究的目的是确定SNP和LDR对肺纤维化的联合作用，并阐明其中的潜在机制。我们使用了SNP诱导的A549细胞和小鼠模型，并通过16S rDNA扩增子测序检测了肠道菌群的改变。此外，还使用苏木和曙红（H＆E）染色，免疫荧光（IF）染色，qRT-PCR和Western blot分析检测了与肺纤维化相关的参数。组织病理学和IF染色试验表明，小鼠共同暴露于SNP和LDR对肺功能和肺纤维化均具有显着的有害作用，与仅接触SNP或LDR相比。此外，在同时暴露于SNP和LDR后，拟杆菌的丰度显着增加，而Firmicutes的丰度显着下降。从机制上讲，Notch级联在患有肺纤维化和A549细胞的慢性SNP暴露的小鼠中被激活。此外，SNP暴露后，Notch通路相关蛋白在肺中的表达水平均升高。体内和体外。值得注意的是，SNP诱导的肠道菌群失调通过触发Notch途径促进了肺上皮损伤，从而导致SNP诱导的肺纤维化。但是，口服益生菌可以保护小鼠免受SNP诱导的肺损伤。我们的研究结果强烈表明，肠道微生物群依赖的Notch途径的激活对SNP和LDR的共同暴露会导致体内肺上皮损伤。补充益生菌是预防SNP和LDR诱导的肺纤维化的潜在方法。
更新日期：2020-11-27
中文翻译：
暴露于二氧化硅纳米颗粒和低剂量辐射的组合会通过肠道微生物群调节加重小鼠肺纤维化
暴露于二氧化硅纳米颗粒（SNP）会导致肺纤维化并威胁人体健康。然而，尚不清楚低剂量辐射（LDR）暴露是否会加剧SNP诱导的肺功能障碍。因此，我们研究的目的是确定SNP和LDR对肺纤维化的联合作用，并阐明其中的潜在机制。我们使用了SNP诱导的A549细胞和小鼠模型，并通过16S rDNA扩增子测序检测了肠道菌群的改变。此外，还使用苏木和曙红（H＆E）染色，免疫荧光（IF）染色，qRT-PCR和Western blot分析检测了与肺纤维化相关的参数。组织病理学和IF染色试验表明，小鼠共同暴露于SNP和LDR对肺功能和肺纤维化均具有显着的有害作用，与仅接触SNP或LDR相比。此外，在同时暴露于SNP和LDR后，拟杆菌的丰度显着增加，而Firmicutes的丰度显着下降。从机制上讲，Notch级联在患有肺纤维化和A549细胞的慢性SNP暴露的小鼠中被激活。此外，SNP暴露后，Notch通路相关蛋白在肺中的表达水平均升高。体内和体外。值得注意的是，SNP诱导的肠道菌群失调通过触发Notch途径促进了肺上皮损伤，从而导致SNP诱导的肺纤维化。但是，口服益生菌可以保护小鼠免受SNP诱导的肺损伤。我们的研究结果强烈表明，肠道微生物群依赖的Notch途径的激活对SNP和LDR的共同暴露会导致体内肺上皮损伤。补充益生菌是预防SNP和LDR诱导的肺纤维化的潜在方法。
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