Differences in the characteristics and pulmonary toxicity of nano- and micron-sized respirable coal dust.
Differences in the characteristics and pulmonary toxicity of nano- and micron-sized respirable coal dust.
复制标题
纳米级与微米级可吸入煤尘的特性及肺毒性差异
DOI：
10.1186/s12931-022-02120-8
复制
发表时间：
2022-07-30
影响因子：
5.8
通讯作者：
中科院分区：
文献类型：
--
作者：
The characteristics of coal dust (CD) particles affect the inhalation of CD, which causes coal worker’s pneumoconiosis (CWP). CD nanoparticles (CD-NPs, < 500 nm) and micron particles (CD-MPs, < 5 μm) are components of the respirable CD. However, the differences in physicochemical properties and pulmonary toxicity between CD-NPs and CD-MPs remain unclear. CD was analyzed by scanning electron microscopy, Malvern nanoparticle size potentiometer, energy dispersive spectroscopy, infrared spectroscopy, and electron paramagnetic resonance spectroscopy. CCK-8 assay, ELISA, transmission electron microscope, JC-1 staining, reactive oxygen species activity probe, calcium ion fluorescent probe, AO/EB staining, flow cytometry, and western blot were used to determine the differences between CD-NPs and CD-MPs on acute pulmonary toxicity. CCK-8, scratch healing and Transwell assay, hematoxylin–eosin and Masson staining, immunohistochemistry, immunofluorescence, and western blot were applied to examine the effects of CD-NPs and CD-MPs on pneumoconiosis. Analysis of the size distribution of CD revealed that the samples had been size segregated. The carbon content of CD-NPs was greater than that of CD-MPs, and the oxygen, aluminum, and silicon contents were less. In in vitro experiments with A549 and BEAS-2B cells, CD-NPs, compared with CD-MPs, had more inflammatory vacuoles, release of pro-inflammatory cytokines (IL-6, IL-1β, TNFα) and profibrotic cytokines (CXCL2, TGFβ1), mitochondrial damage (reactive oxygen species and Ca2+ levels and decreased mitochondrial membrane potential), and cell death (apoptosis, pyroptosis, and necrosis). CD-NPs-induced fibrosis model cells had stronger proliferation, migration, and invasion than did CD-MPs. In in vivo experiments, lung coefficient, alveolar inflammation score, and lung tissue fibrosis score (mean: 1.1%, 1.33, 1.33) of CD-NPs were higher than those of CD-MPs (mean: 1.3%, 2.67, 2.67). CD-NPs accelerated the progression of pulmonary fibrosis by upregulating the expression of pro-fibrotic proteins and promoting epithelial–mesenchymal transition. The regulatory molecules involved were E-cadherin, N-cadherin, COL-1, COL-3, ZO-1, ZEB1, Slug, α-SMA, TGFβ1, and Vimentin. Stimulation with CD-NPs resulted in more pronounced acute and chronic lung toxicity than did stimulation with CD-MPs. These effects included acute inflammatory response, mitochondrial damage, pyroptosis, and necrosis, and more pulmonary fibrosis induced by epithelial–mesenchymal transition. The online version contains supplementary material available at 10.1186/s12931-022-02120-8.
登录
查看更多内容
影响因子：
3.1
作者：
Liu Y;Lu F;Kang L;Wang Z;Wang Y
通讯作者：
Wang Y
影响因子：
4.8
作者：
Selman, Moises;Pardo, Annie
通讯作者：
Pardo, Annie
DOI：
10.3390/ijerph182111568
发表时间：
2021-11-03
影响因子：
--
作者：
Calderón-Garcidueñas L;Stommel EW;Rajkumar RP;Mukherjee PS;Ayala A
通讯作者：
Ayala A
影响因子：
11.5
作者：
Hariri, Lida P.;Adams, David C.;Suter, Melissa J.
通讯作者：
Suter, Melissa J.
影响因子：
5.2
作者：
Chillappagari, Shashipavan;Garapati, Virajith;Guenther, Andreas
通讯作者：
Guenther, Andreas