Blocking triggering receptor expressed on myeloid cells-1 attenuates lipopolysaccharide-induced acute lung injury via inhibiting NLRP3 inflammasome activation.
Blocking triggering receptor expressed on myeloid cells-1 attenuates lipopolysaccharide-induced acute lung injury via inhibiting NLRP3 inflammasome activation.
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阻断髓样细胞-1上表达的触发受体通过抑制NLRP3炎性体激活减轻脂多糖诱导的急性肺损伤
DOI：
10.1038/srep39473
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发表时间：
2016-12-22
影响因子：
4.6
通讯作者：
Guan CX
中科院分区：
文献类型：
--
作者：
Liu T;Zhou Y;Li P;Duan JX;Liu YP;Sun GY;Wan L;Dong L;Fang X;Jiang JX;Guan CX
Acute lung injury (ALI) is associated with high mortality and uncontrolled inflammation plays a critical role in ALI. TREM-1 is an amplifier of inflammatory response, and is involved in the pathogenesis of many infectious diseases. NLRP3 inflammasome is a member of NLRs family that contributes to ALI. However, the effect of TREM-1 on NLRP3 inflammasome and ALI is still unknown. This study aimed to determine the effect of TREM-1 modulation on LPS-induced ALI and activation of the NLRP3 inflammasome. We showed that LR12, a TREM-1 antagonist peptide, significantly improved survival of mice after lethal doses of LPS. LR12 also attenuated inflammation and lung tissue damage by reducing histopathologic changes, infiltration of the macrophage and neutrophil into the lung, and production of the pro-inflammatory cytokine, and oxidative stress. LR12 decreased expression of the NLRP3, pro-caspase-1 and pro-IL-1β, and inhibited priming of the NLRP3 inflammasome by inhibiting NF-κB. LR12 also reduced the expression of NLRP3 and caspase-1 p10 protein, and secretion of the IL-1β, inhibited activation of the NLRP3 inflammasome by decreasing ROS. For the first time, these data show that TREM-1 aggravates inflammation in ALI by activating NLRP3 inflammasome, and blocking TREM-1 may be a potential therapeutic approach for ALI.
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ROS 介导的 NLRP3 炎症小体活性对于烧伤引起的急性肺损伤至关重要。
影响因子：
4.6
作者：
Han S;Cai W;Yang X;Jia Y;Zheng Z;Wang H;Li J;Li Y;Gao J;Fan L;Hu D
通讯作者：
Hu D
Interleukin-1家族：回到未来。
影响因子：
32.4
作者：
Garlanda C;Dinarello CA;Mantovani A
通讯作者：
Mantovani A
影响因子：
8.7
作者：
Elliott EI;Sutterwala FS
通讯作者：
Sutterwala FS
影响因子：
5.5
作者：
Fukumoto, Jutaro;Fukumoto, Itsuko;Kolliputi, Narasaiah
通讯作者：
Kolliputi, Narasaiah
DOI：
10.4049/jimmunol.1102674
发表时间：
2012-06-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Derive M;Bouazza Y;Sennoun N;Marchionni S;Quigley L;Washington V;Massin F;Max JP;Ford J;Alauzet C;Levy B;McVicar DW;Gibot S
通讯作者：
Gibot S