Particles of different sizes and shapes induce neutrophil necroptosis followed by the release of neutrophil extracellular trap-like chromatin.
Particles of different sizes and shapes induce neutrophil necroptosis followed by the release of neutrophil extracellular trap-like chromatin.
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DOI：
10.1038/s41598-017-15106-0
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发表时间：
2017-11-03
影响因子：
4.6
通讯作者：
Anders HJ
中科院分区：
文献类型：
--
作者：
Desai J;Foresto-Neto O;Honarpisheh M;Steiger S;Nakazawa D;Popper B;Buhl EM;Boor P;Mulay SR;Anders HJ
人体暴露于各种工业、环境或内部来源的颗粒，如石棉、明矾、二氧化硅或尿酸盐、磷酸钙、草酸钙、胱氨酸或胆固醇的晶体。这些颗粒的吞噬清除涉及嗜中性粒细胞和巨噬细胞。在这里，我们报告说，中性粒细胞遇到不同大小和形状的颗粒进行坏死性细胞死亡，与中性粒细胞胞外陷阱（NET）样细胞外DNA的形成相关的过程。在人中性粒细胞中，用坏死抑素-1抑制受体相互作用蛋白激酶（RIPK）-1或用坏死磺胺抑制混合谱系激酶结构域样（MLKL）可消除所有上述颗粒诱导的细胞死亡和相关中性粒细胞胞外DNA释放。在体外用Mlkl缺陷型小鼠嗜中性粒细胞获得了所有颗粒的类似结果。此外，Mlkl缺陷型小鼠在将MSU晶体注射到皮下气囊中后缺乏痛风石形成。这些发现意味着纳米或微米颗粒诱导的中性粒细胞胞外DNA释放是中性粒细胞坏死性凋亡的结果，中性粒细胞坏死性凋亡是由RIPK 1-RIPK 3-MLKL信号传导定义的细胞坏死的调节形式。有趣的是，这一发现在不同的颗粒尺寸和形状中是一致的。RIPK 1-RIPK 3-MLKL信号通路可能代表纳米或微粒相关疾病（晶体病）的潜在治疗靶点。
The human body is exposed to a wide range of particles of industrial, environmental or internal origin such as asbestos, alum, silica or crystals of urate, calcium phosphate, calcium oxalate, cystine or cholesterol. Phagocytic clearance of such particles involves neutrophils and macrophages. Here we report that neutrophils encountering such particles of diverse sizes and shapes undergo necrotic cell death, a process associated with the formation of neutrophil extracellular trap (NET)-like extracellular DNA. In human neutrophils receptor-interacting protein kinase (RIPK)-1 inhibition with necrostatin-1s or mixed lineage kinase domain-like (MLKL) inhibition with necrosulfonamide abrogated cell death and associated-neutrophil extracellular DNA release induced by all of the aforementioned particles. Similar results were obtained with Mlkl-deficient mice neutrophils for all particles in vitro. Furthermore, Mlkl-deficient mice lacked tophus formation upon injection of MSU crystals into subcutaneous air pouches. These findings imply that nano- or microparticle-induced neutrophil extracellular DNA release is the consequence of neutrophil necroptosis, a regulated form of cell necrosis defined by RIPK1-RIPK3-MLKL signaling. Interestingly, this finding was consistent across different particle sizes and shapes. The RIPK1-RIPK3-MLKL signaling pathway may represent a potential therapeutic target in nano- or microparticle-related diseases (crystallopathies).
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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：
4.1
作者：
Rada B
通讯作者：
Rada B
DOI：
10.4049/jimmunol.1301821
发表时间：
2013-12-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Malachowa N;Kobayashi SD;Freedman B;Dorward DW;DeLeo FR
通讯作者：
DeLeo FR
影响因子：
4.4
作者：
Wang, Xiaoliang;He, Zhaoyue;Simon, Hans-Uwe
通讯作者：
Simon, Hans-Uwe
影响因子：
16.6
作者：
Mulay SR;Desai J;Kumar SV;Eberhard JN;Thomasova D;Romoli S;Grigorescu M;Kulkarni OP;Popper B;Vielhauer V;Zuchtriegel G;Reichel C;Bräsen JH;Romagnani P;Bilyy R;Munoz LE;Herrmann M;Liapis H;Krautwald S;Linkermann A;Anders HJ
通讯作者：
Anders HJ