University of Montana, Department of Biomedical and Pharmaceutical Sciences, Center for Environmental Sciences , 32 Campus Drive, Missoula, MT , USA.
Nanotoxicology. 2014 Feb;8(1):17-27. doi: 10.3109/17435390.2012.744110. Epub 2012 Nov 14.
Exposure to certain engineered nanomaterials has been associated with pathological changes in animal models raising concerns about potential human health effects. MWCNT have been reported to activate the NLRP3 inflammasome in vitro, correlating with lung inflammation and pathology, in vivo. In this study, we investigated the role of IL-1 signalling in pulmonary inflammatory responses in WT and IL-1R-/- mice after exposure to MWCNT. The results suggest that MWCNT were effective in inducing acute pulmonary inflammation. Additionally, WT mice demonstrated significant increased airway resistance 24 h post exposure to MWCNT, which was also blocked in the IL-1R-/- mice. In contrast, by 28 days post exposure to MWCNT, the inflammatory response that was initially absent in IL-1R-/- mice was elevated in comparison to the WT mice. These data suggest that IL-1R signalling plays a crucial role in the regulation of MWCNT-induced pulmonary inflammation.
暴露于某些工程纳米材料与动物模型中的病理变化有关,这引起了人们对潜在人类健康影响的关注。MWCNT 已被报道在体外激活 NLRP3 炎性体,与肺部炎症和病理学相关,在体内也是如此。在这项研究中,我们研究了 IL-1 信号在 WT 和 IL-1R-/-小鼠暴露于 MWCNT 后的肺部炎症反应中的作用。结果表明,MWCNT 可有效诱导急性肺部炎症。此外,WT 小鼠在暴露于 MWCNT 后 24 小时表现出明显的气道阻力增加,而这种增加在 IL-1R-/-小鼠中也被阻断。相比之下,在暴露于 MWCNT 28 天后,最初在 IL-1R-/-小鼠中不存在的炎症反应在与 WT 小鼠相比升高。这些数据表明,IL-1R 信号在调节 MWCNT 诱导的肺部炎症中起着关键作用。