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口服维生素 A 补充剂对无特定病原体鸡感染传染性支气管炎病毒后宿主免疫反应的影响。

Effect of oral vitamin A supplementation on host immune response to infectious bronchitis virus infection in specific pathogen-free chicken.

机构信息

College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, PR China; State Key Laboratory for Animal Disease Control and Prevention, Harbin Veterinary Research Institute, the Chinese Academy of Agricultural Sciences, Harbin 150069, PR China.

State Key Laboratory for Animal Disease Control and Prevention, Harbin Veterinary Research Institute, the Chinese Academy of Agricultural Sciences, Harbin 150069, PR China.

出版信息

Poult Sci. 2023 Jul;102(7):102701. doi: 10.1016/j.psj.2023.102701. Epub 2023 Apr 13.

DOI:10.1016/j.psj.2023.102701
PMID:37150176
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10192637/
Abstract

Vitamin A is a fat-soluble vitamin that is a crucial mediator of the immune system. In this study, we evaluated the effect of oral vitamin A supplementation on host immune responses to infectious bronchitis virus (IBV) infection in chickens. Forty 1-day-old specific pathogen-free (SPF) chickens were fed a basal diet and randomly divided into 2 groups (n = 20 birds per group). Chickens in the experimental group were treated orally with vitamin A (dissolved in 0.1 mL soybean oil, at a dose of 8,000 IU per kg diet) daily. Birds in the control group were orally administered 0.1 mL soybean oil without vitamin A until 21 d of age. On d 21 after birth, all chickens were infected with 0.1 mL of 10 50% median embryo infectious dose of a pathogenic IBV strain (CK/CH/LDL/091022) by intraocular and intranasal routes. The results demonstrated that oral vitamin A supplementation did not affect the clinical course of disease and growth performance of SPF chickens. However, vitamin A supplementation increased the IBV-specific IgG serum levels and decreased the viral load in some tissues of IBV-infected chickens. In addition, the results demonstrated that vitamin A supplementation decreased the expression levels of most immune-related molecules in some tissues of IBV-infected chickens. Vitamin A supplementation decreased the mRNA expression levels of some avian β-defensins (AvBD2, 3, 6, 7, 11, and 13) and increased the expression levels of AvBD9 and AvBD12 in some tissues of IBV-infected chickens. Similarly, vitamin A supplementation decreased the mRNA expression levels of some cytokines (interferon-γ, interleukin-1β [IL-1β], and IL-6) and increased the mRNA expression levels of IL-2 in some tissues of IBV-infected chickens. Furthermore, vitamin A supplementation decreased the mRNA expression levels of myeloid differentiation primary response protein 88, nuclear factor-κB p65, toll-like receptor 3, toll-like receptor 7, and CD4. In summary, the present study suggests that vitamin A supplementation enhances the immune function of SPF chickens against IBV infection by inhibiting viral replication, increasing the IBV-specific antibody titer, and suppressing the excessive inflammatory responses to IBV infection.

摘要

维生素 A 是一种脂溶性维生素,是免疫系统的重要介质。在这项研究中,我们评估了口服维生素 A 补充剂对鸡感染传染性支气管炎病毒(IBV)后宿主免疫反应的影响。将 40 只 1 日龄无特定病原体(SPF)鸡用基础日粮喂养,并随机分为 2 组(每组 20 只鸡)。实验组鸡每日口服维生素 A(溶于 0.1 mL 大豆油中,剂量为 8000 IU/kg 日粮)。对照组鸡每日口服 0.1 mL 大豆油,直至 21 日龄。在出生后第 21 天,所有鸡通过眼内和鼻内途径感染 0.1 mL 10 50%的中等胚胎感染剂量致病性 IBV 株(CK/CH/LDL/091022)。结果表明,口服维生素 A 补充剂不会影响 SPF 鸡的疾病临床过程和生长性能。然而,维生素 A 补充剂增加了 IBV 特异性 IgG 血清水平,并降低了 IBV 感染鸡的一些组织中的病毒载量。此外,结果表明,维生素 A 补充剂降低了 IBV 感染鸡的一些组织中大多数免疫相关分子的表达水平。维生素 A 补充剂降低了 IBV 感染鸡的一些组织中某些禽 β-防御素(AvBD2、3、6、7、11 和 13)的 mRNA 表达水平,并增加了 AvBD9 和 AvBD12 的表达水平。同样,维生素 A 补充剂降低了 IBV 感染鸡的一些组织中某些细胞因子(干扰素-γ、白细胞介素-1β [IL-1β]和 IL-6)的 mRNA 表达水平,并增加了 IL-2 的 mRNA 表达水平。此外,维生素 A 补充剂降低了 IBV 感染鸡的髓样分化初级反应蛋白 88、核因子-κB p65、Toll 样受体 3、Toll 样受体 7 和 CD4 的 mRNA 表达水平。综上所述,本研究表明,维生素 A 补充剂通过抑制病毒复制、增加 IBV 特异性抗体滴度和抑制对 IBV 感染的过度炎症反应来增强 SPF 鸡对 IBV 感染的免疫功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9122/10192637/707b0d778a28/gr7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9122/10192637/52201958fa84/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9122/10192637/e53e4aefe545/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9122/10192637/923728605738/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9122/10192637/b19c1edb59da/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9122/10192637/707b0d778a28/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9122/10192637/e3565f2bded9/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9122/10192637/73cb18e2a6ae/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9122/10192637/52201958fa84/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9122/10192637/e53e4aefe545/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9122/10192637/923728605738/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9122/10192637/b19c1edb59da/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9122/10192637/707b0d778a28/gr7.jpg

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