IL-1R signalling is critical for regulation of multi-walled carbon nanotubes-induced acute lung inflammation in C57Bl/6 mice.
IL-1R signalling is critical for regulation of multi-walled carbon nanotubes-induced acute lung inflammation in C57Bl/6 mice.
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DOI：
10.3109/17435390.2012.744110
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发表时间：
2014-02
期刊：
影响因子：
5
通讯作者：
Holian A
中科院分区：
文献类型：
--
作者：
Girtsman TA;Beamer CA;Wu N;Buford M;Holian A
接触某些工程纳米材料与动物模型的病理变化有关，引起了对潜在人类健康影响的担忧。据报道，MWCNT在体外激活NLRP 3炎性体，与体内肺部炎症和病理学相关。在这项研究中，我们研究了IL-1信号转导在WT和IL-1 R −/−小鼠暴露于MWCNT后肺部炎症反应中的作用。结果表明，多壁碳纳米管是有效的诱导急性肺部炎症。此外，WT小鼠在暴露于MWCNT后24小时表现出显著增加的气道阻力，这在IL-1 R −/−小鼠中也被阻断。相比之下，在暴露于MWCNT后28天，与WT小鼠相比，IL-1 R −/−小鼠中最初不存在的炎症反应升高。这些数据表明，IL-1 R信号在MWCNT诱导的肺部炎症的调节中起着至关重要的作用。
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.
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影响因子：
29.7
作者：
Davis BK;Wen H;Ting JP
通讯作者：
Ting JP
影响因子：
10
作者：
Hamilton RF;Wu N;Porter D;Buford M;Wolfarth M;Holian A
通讯作者：
Holian A
DOI：
10.4049/jimmunol.0903937
发表时间：
2010-05-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
He X;Mekasha S;Mavrogiorgos N;Fitzgerald KA;Lien E;Ingalls RR
通讯作者：
Ingalls RR
影响因子：
3.3
作者：
Foster, WM;Walters, DM;Miller, LM
通讯作者：
Miller, LM
影响因子：
3.5
作者：
Chen, Chang-Hsiao;Su, Huan-Chieh;Yao, Da-Jeng
通讯作者：
Yao, Da-Jeng