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断奶仔猪F18抗性的调控及其分子机制

Regulation and Molecular Mechanism of on Resistance to F18 in Weaned Piglets.

作者信息

Dai Chaohui, Yang Li, Jin Jian, Wang Haifei, Wu Shenglong, 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). 2019 Sep 27;9(10):735. doi: 10.3390/ani9100735.

DOI:10.3390/ani9100735
PMID:31569693
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6827021/
Abstract

Toll-like receptor 5 (TLR5) plays an important role in immune system. In this study, we performed transcriptome analysis of the duodenum in F18-resistant and -sensitive Sutai weaned piglets and analyzed the differential expression of . The cellular localization of TLR5 was investigated, and the effect of expression on invasion was evaluated after pig small intestinal epithelial cell lines (IPEC-J2) were stimulated by . The results showed that TLR5 expression level in duodenum and jejunum were significantly higher in F18-sensitive than in F18-resistant piglets. TLR5 protein was mainly expressed in the cytoplasm and cell membrane. The expression of genes associated with the TLR5 signaling pathway were significantly higher in -overexpressed cells than in control cells. Bacterial adhesion was higher in -overexpressed cells than in blank cells and lower in interference than in blank cells. The core promoter region of included two CpG islands and 16 acting elements. The methylation of the mC-6 site in the second CpG island of the promoter region had a regulatory effect on expression. Therefore, plays an important regulatory role on invasion. Low expression of inhibited the immune response and decreased cell damage, which was conducive to the resistance to stimulation. In conclusion, this study preliminarily revealed the molecular mechanism of gene regulating the resistance of piglets to , and provided a new candidate gene for screening resistance markers in pigs.

摘要

Toll样受体5(TLR5)在免疫系统中发挥重要作用。在本研究中,我们对F18抗性和敏感苏太断奶仔猪的十二指肠进行了转录组分析,并分析了[具体内容缺失]的差异表达。研究了TLR5的细胞定位,并在猪小肠上皮细胞系(IPEC-J2)受到[具体刺激因素缺失]刺激后,评估了[具体内容缺失]表达对[具体病原体缺失]侵袭的影响。结果表明,F18敏感仔猪十二指肠和空肠中TLR5表达水平显著高于F18抗性仔猪。TLR5蛋白主要在细胞质和细胞膜中表达。与TLR5信号通路相关的基因在[具体基因缺失]过表达细胞中的表达显著高于对照细胞。[具体基因缺失]过表达细胞中的细菌黏附高于空白细胞,而[具体基因缺失]干扰细胞中的细菌黏附低于空白细胞。[具体基因缺失]的核心启动子区域包含两个CpG岛和16个作用元件。启动子区域第二个CpG岛中mC-6位点的甲基化对[具体基因缺失]表达具有调节作用。因此,[具体基因缺失]对[具体病原体缺失]侵袭起着重要的调节作用。[具体基因缺失]的低表达抑制免疫反应并减少细胞损伤,这有利于抵抗[具体病原体缺失]刺激。总之,本研究初步揭示了[具体基因缺失]基因调控仔猪对[具体病原体缺失]抗性的分子机制,并为筛选猪[具体病原体缺失]抗性标记提供了一个新的候选基因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3a8/6827021/2b644a00de0a/animals-09-00735-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3a8/6827021/52adb73df659/animals-09-00735-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3a8/6827021/4ee041613c14/animals-09-00735-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3a8/6827021/79d1d04e2afd/animals-09-00735-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3a8/6827021/e6d73cd59133/animals-09-00735-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3a8/6827021/c9ef2111b588/animals-09-00735-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3a8/6827021/b053b03e2aae/animals-09-00735-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3a8/6827021/2b644a00de0a/animals-09-00735-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3a8/6827021/52adb73df659/animals-09-00735-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3a8/6827021/4ee041613c14/animals-09-00735-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3a8/6827021/79d1d04e2afd/animals-09-00735-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3a8/6827021/e6d73cd59133/animals-09-00735-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3a8/6827021/c9ef2111b588/animals-09-00735-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3a8/6827021/b053b03e2aae/animals-09-00735-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3a8/6827021/2b644a00de0a/animals-09-00735-g007.jpg

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Comprehensive Analysis Revealed the Potential Roles of N-Methyladenosine (mA) Mediating F18 Susceptibility in IPEC-J2 Cells.综合分析揭示了 N6-甲基腺苷(m6A)在 IPEC-J2 细胞中介导 F18 易感性的潜在作用。
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