Oxidative Burst-Dependent NETosis Is Implicated in the Resolution of Necrosis-Associated Sterile Inflammation.
Oxidative Burst-Dependent NETosis Is Implicated in the Resolution of Necrosis-Associated Sterile Inflammation.
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DOI：
10.3389/fimmu.2016.00557
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发表时间：
2016
影响因子：
7.3
通讯作者：
Munoz LE
中科院分区：
文献类型：
--
作者：
Biermann MH;Podolska MJ;Knopf J;Reinwald C;Weidner D;Maueröder C;Hahn J;Kienhöfer D;Barras A;Boukherroub R;Szunerits S;Bilyy R;Hoffmann M;Zhao Y;Schett G;Herrmann M;Munoz LE
坏死与严重的炎症反应有关。坏死相关炎症的调节，特别是负责炎症消退的机制尚未完全表征。已知纳米颗粒诱导质膜损伤和坏死，随后是无菌炎症。我们观察到，注射代谢惰性纳米金刚石导致WT和Ncf 1 ** 小鼠的爪水肿。然而，虽然WT小鼠中的炎症迅速消退，但在Ncf 1 ** 小鼠中持续数周，表明炎症消退失败。从机制上讲，NOX 2依赖性活性氧（ROS）的产生和中性粒细胞胞外陷阱的形成对于解决坏死诱导的炎症至关重要：因此，通过评估炎症部位颗粒的命运，我们观察到NADPH依赖性ROS缺陷的Ncf 1 ** 小鼠无法产生肉芽组织，因此无法捕获纳米金刚石。这些数据表明，N0X2依赖性NETosis通过在坏死组织和健康周围组织之间形成NETosis依赖性屏障，对于防止对组织坏死的炎症反应的慢性化至关重要。
Necrosis is associated with a profound inflammatory response. The regulation of necrosis-associated inflammation, particularly the mechanisms responsible for resolution of inflammation is incompletely characterized. Nanoparticles are known to induce plasma membrane damage and necrosis followed by sterile inflammation. We observed that injection of metabolically inert nanodiamonds resulted in paw edema in WT and Ncf1** mice. However, while inflammation quickly resolved in WT mice, it persisted over several weeks in Ncf1** mice indicating failure of resolution of inflammation. Mechanistically, NOX2-dependent reactive oxygen species (ROS) production and formation of neutrophil extracellular traps were essential for the resolution of necrosis-induced inflammation: hence, by evaluating the fate of the particles at the site of inflammation, we observed that Ncf1** mice deficient in NADPH-dependent ROS failed to generate granulation tissue therefore being unable to trap the nanodiamonds. These data suggest that NOX2-dependent NETosis is crucial for preventing the chronification of the inflammatory response to tissue necrosis by forming NETosis-dependent barriers between the necrotic and healthy surrounding tissue.
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DOI：
10.1084/jem.20100239
发表时间：
2010-08-30
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Li P;Li M;Lindberg MR;Kennett MJ;Xiong N;Wang Y
通讯作者：
Wang Y
影响因子：
17.1
作者：
Huang K;Ma H;Liu J;Huo S;Kumar A;Wei T;Zhang X;Jin S;Gan Y;Wang PC;He S;Zhang X;Liang XJ
通讯作者：
Liang XJ
影响因子：
5.4
作者：
Desai, Jyaysi;Kumar, Santhosh V.;Anders, Hans-Joachim
通讯作者：
Anders, Hans-Joachim
影响因子：
17.1
作者：
Bartneck, Matthias;Keul, Heidrun A.;Groll, Juergen
通讯作者：
Groll, Juergen
在细胞死亡和炎症的串扰中进行了编程坏死。
影响因子：
29.7
作者：
Chan FK;Luz NF;Moriwaki K
通讯作者：
Moriwaki K