Activation of ChTLR15/ChNF-κB-ChNLRP3/ChIL-1β signaling transduction pathway mediated inflammatory responses to E. tenella infection.

Activation of ChTLR15/ChNF-κB-ChNLRP3/ChIL-1β signaling transduction pathway mediated inflammatory responses to E. tenella infection.
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DOI:
10.1186/s13567-020-00885-8
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发表时间:
2021-01-29
影响因子:
4.4
通讯作者:
Ma D
Ma D
中科院分区:
农林科学2区
文献类型:
--
作者:
Li J;Yang X;Jia Z;Ma C;Pan X;Ma D

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由艾美耳球虫引起的鸡球虫病给全球养禽业造成了严重的经济损失。虽然鸡Toll样受体15(ChTLR 15)被报道参与艾美耳球虫感染,其在炎症反应中的作用的详细机制仍有待发现。结果表明,感染鸡盲肠组织中ChTLR 15、ChMyD 88、ChNF-κB、ChNLRP 3、ChCaspase-1、ChIL-18和ChIL-1β的mRNA表达水平以及ChTLR 15和ChNLRP 3的蛋白表达水平在4、12和24 h均显著高于对照鸡(p < 0.01)。此外,在E.柔嫩艾美耳球虫子孢子与艾美耳球虫感染鸡的子孢子一致。此外,ChTLR 15在DF 1细胞中的过表达增强了E. tenella子孢子,而DF 1细胞中ChTLR 15的敲低则表现出相反的效果。综上所述,本研究提供的证据表明,E。柔嫩艾美耳球虫子孢子特异性激活ChTLR 15,然后触发ChNLRP 3/ChIL-1β途径的激活,该途径部分介导对艾美耳球虫感染的炎症反应。
Avian coccidiosis caused by Eimeria leads to severe economic losses in the global poultry industry. Although chicken Toll-like receptor 15 (ChTLR15) was reported to be involved in Eimeria infection, the detailed mechanism underlying its role in the inflammatory response remains to be discovered. The present study demonstrated that the mRNA expression levels of ChTLR15, ChMyD88, ChNF-κB, ChNLRP3, ChCaspase-1, ChIL-18 and ChIL-1β and the protein levels of ChTLR15 and ChNLRP3 in cecal tissues of Eimeria-infected chickens were significantly elevated at 4, 12, and 24 h compared with those in noninfected control chickens (p < 0.01). Moreover, the mRNA levels of molecules in the ChTLR15/ChNF-κB and ChNLRP3/ChIL-1β pathways and the protein levels of ChTLR15 and ChNLRP3 in chicken embryo fibroblast cells (DF-1) stimulated by E. tenella sporozoites were consistent with those in Eimeria-infected chickens. Furthermore, overexpression of ChTLR15 in DF1 cells augmented activation of the ChTLR15/ChNF-κB and ChNLRP3/ChIL-1β pathways when stimulated with E. tenella sporozoites, while knockdown of ChTLR15 in DF1 cells showed inverse effects. Taken together, the present study provides evidence that E. tenella sporozoites specifically activate ChTLR15 and then trigger activation of the ChNLRP3/ChIL-1β pathway, which partially mediates inflammatory responses to Eimeria infection.
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