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表达对猪肾细胞中F18感染的影响。

The Impact of Expression on F18 Infection in Porcine Kidney Cells.

作者信息

Jin Jian, Huang Yanjie, Sun Shouyong, Wu Zhengchang, Wu Shenglong, Yin Zongjun, Bao Wenbin

机构信息

Key Laboratory for Animal Genetics, Breeding, Reproduction and Molecular Design, College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.

Joint International Research Laboratory of Agriculture & Agri-Product Safety, Yangzhou University, Yangzhou 225009, China.

出版信息

Animals (Basel). 2020 Nov 15;10(11):2118. doi: 10.3390/ani10112118.

DOI:10.3390/ani10112118
PMID:33203175
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7696536/
Abstract

The efficacy and regulatory activity of bactericidal/permeability-increasing protein () as a mediator of () F18 resistance remains to be defined. In the present study, we evaluated lipopolysaccharide (LPS)-induced changes in gene expression in porcine kidney (PK15) cells in response to F18 exposure. We additionally generated PK15 cells that overexpressed to assess the impact of this gene on Toll-like receptor 4 (TLR4) signaling and glycosphingolipid biosynthesis-related genes. Through these analyses, we found that expression rose significantly following LPS exposure in response to F18ac stimulation ( < 0.01). Colony count assays and qPCR analyses revealed that F18 adherence to PK15 cells was markedly suppressed following overexpression ( < 0.01). overexpression had no significant effect on the mRNA-level expression of genes associated with glycosphingolipid biosynthesis or TLR4 signaling. overexpression suppressed the LPS-induced TLR4 signaling pathway-related expression of proinflammatory cytokines (, , , and ). Overall, our study serves as an overview of the association between and resistance to F18 at the cellular level, offering a framework for future investigations of the mechanisms whereby piglets are able to resist F18 infection.

摘要

杀菌/通透性增加蛋白()作为介导猪源大肠杆菌F18抗性的介质,其功效和调节活性仍有待确定。在本研究中,我们评估了脂多糖(LPS)诱导的猪肾(PK15)细胞中基因表达的变化,以响应F18暴露。我们还构建了过表达的PK15细胞,以评估该基因对Toll样受体4(TLR4)信号传导和糖鞘脂生物合成相关基因的影响。通过这些分析,我们发现,在F18ac刺激下,LPS暴露后表达显著上升(<0.01)。菌落计数分析和qPCR分析表明,过表达后,F18对PK15细胞的粘附明显受到抑制(<0.01)。过表达对与糖鞘脂生物合成或TLR4信号传导相关的基因的mRNA水平表达没有显著影响。过表达抑制了LPS诱导的促炎细胞因子(、、、和)的TLR4信号通路相关表达。总的来说,我们的研究概述了在细胞水平上与对F18抗性之间的关联,为未来研究仔猪抵抗F18感染的机制提供了一个框架。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a2/7696536/0a1fe6b773b9/animals-10-02118-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a2/7696536/2f74e8443cdf/animals-10-02118-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a2/7696536/79f55a0f3e55/animals-10-02118-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a2/7696536/fc114e629ac0/animals-10-02118-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a2/7696536/accb95d0e1ef/animals-10-02118-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a2/7696536/0a1fe6b773b9/animals-10-02118-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a2/7696536/2f74e8443cdf/animals-10-02118-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a2/7696536/79f55a0f3e55/animals-10-02118-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a2/7696536/fc114e629ac0/animals-10-02118-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a2/7696536/accb95d0e1ef/animals-10-02118-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a2/7696536/0a1fe6b773b9/animals-10-02118-g005.jpg

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本文引用的文献

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Transcriptome analysis of PK-15 cells in innate immune response to porcine deltacoronavirus infection.猪德尔塔冠状病毒感染诱导 PK-15 细胞固有免疫反应的转录组分析。
PLoS One. 2019 Oct 1;14(10):e0223177. doi: 10.1371/journal.pone.0223177. eCollection 2019.
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Mapping the neutralizing epitopes of F18 fimbrial adhesin subunit FedF of enterotoxigenic Escherichia coli (ETEC).绘制肠致病性大肠杆菌(ETEC)F18 菌毛黏附亚单位 FedF 的中和表位图谱。
Vet Microbiol. 2019 Mar;230:171-177. doi: 10.1016/j.vetmic.2019.02.015. Epub 2019 Feb 6.
3
New Insight into the Molecular Mechanism of the Regulating F18 Resistance in Weaned Piglets.
断奶仔猪 F18 耐药性调控的分子机制新见解。
Int J Mol Sci. 2018 Oct 24;19(11):3301. doi: 10.3390/ijms19113301.
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Crystal structure of the mouse innate immunity factor bacterial permeability-increasing family member A1.小鼠固有免疫因子细菌通透性增加家族成员A1的晶体结构
Acta Crystallogr F Struct Biol Commun. 2018 May 1;74(Pt 5):268-276. doi: 10.1107/S2053230X18004600. Epub 2018 Apr 16.
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Identification of the RNA Pseudoknot within the 3' End of the Porcine Reproductive and Respiratory Syndrome Virus Genome as a Pathogen-Associated Molecular Pattern To Activate Antiviral Signaling via RIG-I and Toll-Like Receptor 3.鉴定猪繁殖与呼吸综合征病毒基因组 3' 末端的 RNA 假结作为一种病原体相关分子模式,通过 RIG-I 和 Toll 样受体 3 激活抗病毒信号。
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