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

被引:12
作者
Ma, Bin [1 ,2 ]
Hua, Kexin [1 ]
Zhou, Shanshan [1 ]
Zhou, Hufeng [3 ,4 ]
Chen, Yushan [1 ]
Luo, Rui [1 ,5 ]
Bi, Dingren [1 ]
Zhou, Rui [1 ,5 ]
He, Qigai [1 ,5 ]
Jin, Hui [1 ]
机构
[1] Huazhong Agr Univ, Coll Vet Med, State Key Lab Agr Microbiol, Wuhan 430070, Hubei, Peoples R China
[2] Huazhong Agr Univ, Coll Life Sci & Technol, Wuhan 430070, Hubei, Peoples R China
[3] Brigham & Womens Hosp, Dept Med, 75 Francis St, Boston, MA 02115 USA
[4] Harvard Med Sch, Dept Microbiol & Immunobiol, Boston, MA 02115 USA
[5] Cooperat Innovat Ctr Sustainable Pig Prod, Wuhan 430070, Hubei, Peoples R China
基金
中国国家自然科学基金;
关键词
Haemophilus parasuis; NOD1/2; NF-kappa B; Inflammatory cytokine; NF-KAPPA-B; INTESTINAL EPITHELIAL-CELLS; TOLL-LIKE RECEPTORS; NOD-LIKE RECEPTORS; HOST-DEFENSE; INFLAMMATORY DISEASE; ENDOTHELIAL-CELLS; INNATE; RECOGNITION; RANTES;
D O I
10.1016/j.dci.2017.10.021
中图分类号
S9 [水产、渔业];
学科分类号
0908 ;
摘要
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-kappa B activity, while the phosphorylation level of p38, JNK or ERIC 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. (C) 2017 Elsevier Ltd. All rights reserved.
引用
收藏
页码:158 / 165
页数:8
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