IL-1R signalling is critical for regulation of multi-walled carbon nanotubes-induced acute lung inflammation in C57Bl/6 mice

被引:40
作者
Girtsman, Teri Alyn [1 ]
Beamer, Celine A. [1 ]
Wu, Nianqiang [2 ]
Buford, Mary [1 ]
Holian, Andrij [1 ]
机构
[1] Univ Montana, Ctr Environm Sci, Dept Biomed & Pharmaceut Sci, Missoula, MT 59812 USA
[2] W Virginia Univ, Dept Mech & Aerosp Engn, Morgantown, WV 26506 USA
关键词
nanotubes; nanotoxicology; environmental toxicology; particle characterisation; TNF-ALPHA RECEPTOR; NALP3; INFLAMMASOME; PULMONARY-FUNCTION; INTERLEUKIN-1; RESPONSES; TOXICITY; AIRWAY; MYD88; ACTIVATION; MEDIATORS;
D O I
10.3109/17435390.2012.744110
中图分类号
TB3 [工程材料学];
学科分类号
0805 ; 080502 ;
摘要
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.
引用
收藏
页码:17 / 27
页数:11
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