High dose of dietary vitamin D3 modulated the yellow catfish (Pelteobagrus fulvidraco) splenic innate immune response after Edwardsiella ictaluri infection

High dose of dietary vitamin D3 modulated the yellow catfish (Pelteobagrus fulvidraco) splenic innate immune response after Edwardsiella ictaluri infection
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高剂量膳食维生素 D3 调节鲶鱼爱德华氏菌感染后黄颡鱼 (Pelteobagrus fulvidraco) 脾脏的先天免疫反应

DOI:
10.1016/j.fsi.2020.03.005
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发表时间:
2020-05-01
影响因子:
4.7
通讯作者:
Wang, Chunfang
Wang, Chunfang
中科院分区:
农林科学2区
文献类型:
--
作者:
Cheng, Ke;Tang, Qin;Wang, Chunfang

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相似文献

维生素D-3(VD 3)已被证明可以调节哺乳动物的先天免疫反应,但这在鱼类中很少报道。目前的研究发现,增加膳食维生素D3含量可以降低感染爱德华氏菌的黄鲶鱼脾脏中黄色至深棕色色素巨噬细胞聚集体(PMA)的密度。新一代测序结果显示,高剂量的饲料VD 3(16,600 IU/kg)主要通过负调节“NF-κ B转录因子活性”、“NIK/NF-κ B信号传导”和“i-κ B激酶/NF-κ B信号传导”途径影响感染爱德华氏菌期间的脾脏免疫应答。后续qPCR结果显示,VD 3可增加NF-κ B抑制因子i kappa b-α的表达,降低NF-κ B p65、il-6、il 1-β和TNF-α的表达,下调NIK/NF-κ B信号通路中nik、ikks和NF-κ B p52的表达。以上结果表明,饲料VD(3)()可通过抑制NF-κ B B活化信号通路,调节黄颡鱼感染爱德华氏菌后脾脏的天然免疫应答。
Vitamin D-3 (VD3) has been shown to modulate the innate immune response in mammals but this has been rarely reported in fish. The current study found that increasing dietary VD3 content can reduce the density of yellow to dark brown pigmented macrophage aggregates (PMAs) in the spleens of yellow catfish infected with Edwardsiella ictaluri. The results of next-generation sequencing showed that a high dose of dietary VD3 (16,600 IU/kg) mainly affected the splenic immune response during Edwardsiella ictaluri infection via negative regulation of 'NF-kappa B transcription factor activity', 'NIK/NF-kappa B signaling' and the 'i-kappab kinase/NF-kappa B signaling' pathways. Followup qPCR showed that dietary VD3 increased the expression of NF-kappa B inhibitor i kappa b-alpha, decreased the expression of nf-kappa b p65, il-6, il1-beta and tnf-alpha, and down-regulated the expression of nik, ikks and nf-kappa b p52 in the NIK/NF-kappaB signaling pathway. The above results indicate that dietary VD(3)( )can modulate the splenic innate immune response of yellow catfish after Edwardsiella ictaluri infection by inhibiting the NF-kappa B activation signaling pathways.