• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

副猪嗜血杆菌感染激活PK-15细胞中的NOD1/2-RIP2信号通路。

Haemophilus parasuis infection activates NOD1/2-RIP2 signaling pathway in PK-15 cells.

作者信息

Ma Bin, Hua Kexin, Zhou Shanshan, Zhou Hufeng, Chen Yushan, Luo Rui, Bi Dingren, Zhou Rui, He Qigai, Jin Hui

机构信息

State Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China; College of Life Science and Technology, Huazhong Agricultural University, Wuhan 430070, Hubei, China.

State Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China.

出版信息

Dev Comp Immunol. 2018 Feb;79:158-165. doi: 10.1016/j.dci.2017.10.021. Epub 2017 Oct 31.

DOI:10.1016/j.dci.2017.10.021
PMID:29097236
Abstract

Haemophilus parasuis, an important swine pathogen, was recently proven able to invade into endothelial or epithelial cell in vitro. NOD1/2 are specialized NLRs that participate in the recognition of pathogens able to invade intracellularly and therefore, we assessed that the contribution of NOD1/2 to inflammation responses during H. parasuis infection. We observed that H. parasuis infection enhanced NOD2 expression and RIP2 phosphorylation in porcine kidney 15 cells. Our results also showed that knock down of NOD1/2 or RIP2 expression respectively significantly decreased H. parasuis-induced NF-κB activity, while the phosphorylation level of p38, JNK or ERK was not changed. Moreover, real-time PCR result showed that NOD1, NOD2 or RIP2 was involved in the expression of CCL4, CCL5 and IL-8. Inhibition of NOD1 and NOD2 significantly reduced CCL5 promoter activity, even in a more effective way compared with inhibition of TLR.

摘要

副猪嗜血杆菌是一种重要的猪病原体,最近被证实能够在体外侵入内皮细胞或上皮细胞。NOD1/2是专门的NLRs,参与识别能够侵入细胞内的病原体,因此,我们评估了NOD1/2在副猪嗜血杆菌感染期间对炎症反应的作用。我们观察到副猪嗜血杆菌感染增强了猪肾15细胞中NOD2的表达和RIP2的磷酸化。我们的结果还表明,分别敲低NOD1/2或RIP2的表达显著降低了副猪嗜血杆菌诱导的NF-κB活性,而p38、JNK或ERK的磷酸化水平没有改变。此外,实时PCR结果表明,NOD1、NOD2或RIP2参与了CCL4、CCL5和IL-8的表达。抑制NOD1和NOD2显著降低了CCL5启动子活性,甚至比抑制TLR更有效。

相似文献

1
Haemophilus parasuis infection activates NOD1/2-RIP2 signaling pathway in PK-15 cells.副猪嗜血杆菌感染激活PK-15细胞中的NOD1/2-RIP2信号通路。
Dev Comp Immunol. 2018 Feb;79:158-165. doi: 10.1016/j.dci.2017.10.021. Epub 2017 Oct 31.
2
The Nod1, Nod2, and Rip2 axis contributes to host immune defense against intracellular Acinetobacter baumannii infection.Nod1、Nod2 和 Rip2 轴有助于宿主对细胞内鲍曼不动杆菌感染的免疫防御。
Infect Immun. 2014 Mar;82(3):1112-22. doi: 10.1128/IAI.01459-13. Epub 2013 Dec 23.
3
XIAP mediates NOD signaling via interaction with RIP2.X连锁凋亡抑制蛋白(XIAP)通过与受体相互作用蛋白2(RIP2)相互作用介导核苷酸结合寡聚化结构域样受体(NOD)信号传导。
Proc Natl Acad Sci U S A. 2009 Aug 25;106(34):14524-9. doi: 10.1073/pnas.0907131106. Epub 2009 Aug 10.
4
A critical role of RICK/RIP2 polyubiquitination in Nod-induced NF-kappaB activation.RICK/RIP2多聚泛素化在Nod诱导的NF-κB激活中的关键作用。
EMBO J. 2008 Jan 23;27(2):373-83. doi: 10.1038/sj.emboj.7601962. Epub 2007 Dec 13.
5
Haemophilus parasuis induces activation of NF-κB and MAP kinase signaling pathways mediated by toll-like receptors.副猪嗜血杆菌可诱导由Toll样受体介导的NF-κB和丝裂原活化蛋白激酶信号通路的激活。
Mol Immunol. 2015 Jun;65(2):360-6. doi: 10.1016/j.molimm.2015.02.016. Epub 2015 Feb 28.
6
Activation of the nucleotide oligomerization domain signaling pathway by the non-bacterially derived xanthone drug 5'6-dimethylxanthenone-4-acetic acid (Vadimezan).非细菌来源的黄烷酮类药物 5'6-二甲基黄烷酮-4-乙酸(Vadimezan)激活核苷酸寡聚化结构域信号通路。
J Biol Chem. 2010 Apr 2;285(14):10553-62. doi: 10.1074/jbc.M109.065631. Epub 2010 Jan 29.
7
Nod1 and Nod2 induce CCL5/RANTES through the NF-kappaB pathway.Nod1和Nod2通过NF-κB途径诱导CCL5/趋化因子调节激活正常T细胞表达和分泌因子。
Eur J Immunol. 2007 Sep;37(9):2499-508. doi: 10.1002/eji.200737069.
8
Autophagy Is a Defense Mechanism Inhibiting Invasion and Inflammation During High-Virulent Infection in PK-15 Cells.自噬是一种防御机制,可抑制高毒力感染期间 PK-15 细胞的侵袭和炎症反应。
Front Cell Infect Microbiol. 2019 Apr 16;9:93. doi: 10.3389/fcimb.2019.00093. eCollection 2019.
9
Structural and functional insights into CARDs of zebrafish (Danio rerio) NOD1 and NOD2, and their interaction with adaptor protein RIP2.斑马鱼(Danio rerio)NOD1和NOD2的CARD结构与功能解析,以及它们与衔接蛋白RIP2的相互作用
Mol Biosyst. 2015 Aug;11(8):2324-36. doi: 10.1039/c5mb00212e.
10
E-selectin expression induced by Porphyromonas gingivalis in human endothelial cells via nucleotide-binding oligomerization domain-like receptors and Toll-like receptors.牙龈卟啉单胞菌通过核苷酸结合寡聚化结构域样受体和Toll样受体诱导人内皮细胞中E-选择素的表达。
Mol Oral Microbiol. 2015 Oct;30(5):399-410. doi: 10.1111/omi.12102. Epub 2015 Jun 24.

引用本文的文献

1
HbpA from Glaesserella parasuis induces an inflammatory response in 3D4/21 cells by activating the MAPK and NF-κB signalling pathways and protects mice against G. parasuis when used as an immunogen.副猪嗜血杆菌 HbpA 通过激活 MAPK 和 NF-κB 信号通路诱导 3D4/21 细胞炎症反应,并作为免疫原保护小鼠抵抗副猪嗜血杆菌感染。
Vet Res. 2024 Jul 29;55(1):93. doi: 10.1186/s13567-024-01344-4.
2
Polyamine Transport Protein PotD Protects Mice against and Elevates the Secretion of Pro-Inflammatory Cytokines of Macrophage via JNK-MAPK and NF-κB Signal Pathways through TLR4.多胺转运蛋白PotD通过TLR4经由JNK-MAPK和NF-κB信号通路保护小鼠免受侵害并提高巨噬细胞促炎细胞因子的分泌。
Vaccines (Basel). 2019 Dec 14;7(4):216. doi: 10.3390/vaccines7040216.
3
Surface-exposed loops L7 and L8 of Haemophilus (Glaesserella) parasuis OmpP2 contribute to the expression of proinflammatory cytokines in porcine alveolar macrophages.猪胸膜肺炎放线杆菌 OmpP2 的表面暴露环 L7 和 L8 有助于猪肺泡巨噬细胞中促炎细胞因子的表达。
Vet Res. 2019 Nov 29;50(1):105. doi: 10.1186/s13567-019-0721-4.
4
Autophagy Is a Defense Mechanism Inhibiting Invasion and Inflammation During High-Virulent Infection in PK-15 Cells.自噬是一种防御机制,可抑制高毒力感染期间 PK-15 细胞的侵袭和炎症反应。
Front Cell Infect Microbiol. 2019 Apr 16;9:93. doi: 10.3389/fcimb.2019.00093. eCollection 2019.