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Silica dioxide nanoparticles aggravate airway inflammation in an asthmatic mouse model via NLRP3 inflammasome activation.
Regulatory Toxicology and Pharmacology ( IF 3.0 ) Pub Date : 2020-02-19 , DOI: 10.1016/j.yrtph.2020.104618
Je-Won Ko 1 , Na-Rae Shin 2 , Lim Je-Oh 2 , Tae-Yang Jung 2 , Changjong Moon 2 , Tae-Won Kim 3 , Jungil Choi 4 , In-Sik Shin 2 , Jeong-Doo Heo 4 , Jong-Choon Kim 2
Affiliation  

Silica dioxide nanoparticles (SiONPs) are mainly used in the rubber industry; however, they are a major air pollutant in Asia. Thus, extensive research on this issue is required. In this study, we investigated the effects of SiONPs on asthma aggravation and elucidated the underlying mechanism using ovalbumin (OVA)-induced asthmatic mice model and in NCI-H292 cells. Mice exposed to SiONPs showed markedly increased Penh values, inflammatory cell counts, and inflammatory cytokine levels compared to OVA-induced asthmatic mice. Exposure to SiONPs also induced additional airway inflammation and mucus secretion with increases in protein expression levels of thioredoxin-interacting protein (TXNIP), NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome, and interleukin (IL)-1β compared to those in OVA-induced asthmatic mice. Treatment of SiONPs in NCI-H292 cells also significantly increased mRNA expression levels of inflammatory cytokines accompanied with elevation in the levels of TXNIP, NLRP3 inflammasome, and IL-1β proteins in a concentration-dependent manner. Taken together, exposure to SiONPs aggravated asthma development, which is closely related to inflammasome activation. Our results provide useful information about the toxicological effects of SiONPs on asthma exacerbation and suggest the need to avoid SiONP exposure especially in individuals with respiratory diseases.

中文翻译:

二氧化硅纳米颗粒通过NLRP3炎症小体激活加重哮喘小鼠模型中的气道炎症。

二氧化硅纳米粒子(SiONPs)主要用于橡胶工业;但是,它们是亚洲的主要空气污染物。因此,需要对该问题进行广泛的研究。在这项研究中,我们调查了SiONPs对哮喘加重的影响,并阐明了使用卵清蛋白(OVA)诱导的哮喘小鼠模型和NCI-H292细胞的潜在机制。与OVA诱发的哮喘小鼠相比,接触SiONPs的小鼠显示出明显的Penh值,炎性细胞计数和炎性细胞因子水平升高。与那些相比,暴露于SiONPs还会诱导更多的气道炎症和粘液分泌,其中硫氧还蛋白相互作用蛋白(TXNIP),含NOD样受体吡啶结构域的3(NLRP3)炎性小体和白介素(IL)-1β的蛋白表达水平增加。在OVA诱发的哮喘小鼠中。NCI-H292细胞中SiONP的处理还以浓度依赖的方式显着增加了炎症细胞因子的mRNA表达水平,并伴随着TXNIP,NLRP3炎性小体和IL-1β蛋白水平的升高。综上所述,接触SiONPs会加剧哮喘的发展,这与炎症小体的活化密切相关。我们的研究结果提供了有关SiONPs对哮喘加重的毒理作用的有用信息,并建议需要避免SiONPs暴露,尤其是在患有呼吸系统疾病的个体中。这与炎症小体激活密切相关。我们的研究结果提供了有关SiONPs对哮喘加重的毒理作用的有用信息,并建议需要避免SiONPs暴露,尤其是在患有呼吸系统疾病的个体中。这与炎症小体激活密切相关。我们的研究结果提供了有关SiONPs对哮喘加重的毒理作用的有用信息,并建议需要避免SiONPs暴露,尤其是在患有呼吸系统疾病的个体中。
更新日期:2020-02-20
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