S1PR1 regulates NDV-induced IL-1β expression via NLRP3/caspase-1 inflammasome.
S1PR1 regulates NDV-induced IL-1β expression via NLRP3/caspase-1 inflammasome.
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S1PR1 通过 NLRP3/caspase-1 炎性体调节 NDV 诱导的 IL-1β 表达
DOI：
10.1186/s13567-022-01078-1
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发表时间：
2022-07-19
影响因子：
4.4
通讯作者：
中科院分区：
文献类型：
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作者：
新城疫（ND）是由新城疫病毒（NDV）引起的一种急性、发热性、高度接触性传染病，是危害家禽的重要病原体。 NDV 毒株感染会诱导 IL-1β 表达，并伴随强烈的炎症反应，最终导致死亡。 S1PR1是炎症性疾病治疗的重要靶点，其抑制或过度表达可调节IL-1β的表达，表明S1PR1可能通过调节促炎细胞因子的表达来改变NDV感染诱导的炎症反应的程度。然而，S1PR1调节IL-1β表达的分子机制仍不清楚。在这里，我们探讨了 NDV 感染后 S1PR1 的表达和组织分布，发现 S1PR1 在肺、法氏囊和 DF-1 中表达增加。用 S1PR1 特异性激动剂 SEW2871 处理细胞后，NDV 诱导的 IL-1β 表达增加。相反，用S1PR1抑制剂W146处理细胞后，NDV诱导的IL-1β表达降低，表明S1PR1促进NDV诱导的IL-1β表达。进一步研究表明，NDV通过p38、JNK/MAPK和NLRP3/caspase-1信号分子诱导IL-1β表达，S1PR1通过激活NLRP3/caspase-1炎症小体影响IL-1β表达，但对p38和JNK/MAPK无显着影响。我们的研究表明，NDV感染通过p38、JNK/MAPK和NLRP3/caspase-1炎症小体促进S1PR1表达并诱导IL-1β表达，并且S1PR1主要通过NLRP3/caspase-1炎症小体调节IL-1β表达。
Newcastle disease (ND) is an acute, febrile, and highly contagious disease caused by the Newcastle disease virus (NDV), an important pathogen harmful to domestic poultry. Virulent NDV strain infection induces IL-1β expression and along with strong inflammatory response, ultimately results in death. Inhibition or overexpression of S1PR1, an important target for inflammatory disease treatment, regulates IL-1β expression, suggesting that S1PR1 may alter the degree of the inflammatory response induced by NDV infection by regulating pro-inflammatory cytokine expression. However, the molecular mechanism by which S1PR1 regulates IL-1β expression remains unclear. Here, we explore the expression and tissue distribution of S1PR1 after NDV infection and found that S1PR1 expression increased in the lungs, bursa of Fabricius, and DF-1. IL-1β expression induced by NDV was increased following treatment of cells with the S1PR1-specific agonist, SEW2871. In contrast, IL-1β expression induced by NDV was decreased after cells were treated with the S1PR1 inhibitor W146, suggesting that S1PR1 promotes NDV-induced IL-1β expression. Further investigation demonstrated that NDV induced IL-1β expression through p38, JNK/MAPK, and NLRP3/caspase-1 signaling molecules and S1PR1 affected the expression of IL-1β by activating the NLRP3/caspase-1 inflammasome but had no significant effect on p38 and JNK/MAPK. Our study shows that NDV infection promotes S1PR1 expression and induces IL-1β expression through p38, JNK/MAPK, and NLRP3/caspase-1 inflammasomes and that S1PR1 regulates IL-1β expression mainly through the NLRP3/caspase-1 inflammasome.
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DOI：
10.1084/jem.20160392
发表时间：
2017-09-04
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Weichand B;Popp R;Dziumbla S;Mora J;Strack E;Elwakeel E;Frank AC;Scholich K;Pierre S;Syed SN;Olesch C;Ringleb J;Ören B;Döring C;Savai R;Jung M;von Knethen A;Levkau B;Fleming I;Weigert A;Brüne B
通讯作者：
Brüne B
影响因子：
2.6
作者：
Li R;Guo K;Liu C;Wang J;Tan D;Han X;Tang C;Zhang Y;Wang J
通讯作者：
Wang J
影响因子：
3.8
作者：
Tantikanlayaporn D;Tourkova IL;Larrouture Q;Luo J;Piyachaturawat P;Witt MR;Blair HC;Robinson LJ
通讯作者：
Robinson LJ
VIId基因型新城疫病毒的M、F和HN基因与鸡脾脏的严重病理改变有关。
影响因子：
4.8
作者：
Kai Y;Hu Z;Xu H;Hu S;Zhu J;Hu J;Wang X;Liu X;Liu X
通讯作者：
Liu X
影响因子：
2.7
作者：
Bian, Jianchun;Wang, Kai;Meng, Songshu
通讯作者：
Meng, Songshu