Zhou Yajing, Ren Zhanshi, Zhang Shuai, Wang Haifei, Wu Shenglong, Bao Wenbin
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, The Ministry of Education of China, Yangzhou University, Yangzhou 225009, China.
Animals (Basel). 2021 Mar 1;11(3):644. doi: 10.3390/ani11030644.
Porcine epidemic diarrhea virus (PEDV) infects intestinal epithelial cells, destroys the intestinal mucosal barrier and then causes diarrhea in piglets. Glucagon-like peptide-2 (GLP-2) is a specific intestinal growth hormone that promotes the repair of damaged intestinal mucosa and improves the intestinal barrier. In this study, we investigated the functions of porcine gene in regulating PEDV infection. The intestinal tissues with damaged intestinal structures caused by PEDV infection were first confirmed and collected. Expression analysis indicated that the gene was expressed in the duodenum, jejunum and ileum tissues, and the mRNA level was significantly down-regulated in jejunum and ileum of piglets with damaged intestinal mucosa. Infection of PEDV to porcine small intestinal epithelial cells in vitro showed that gene was significantly decreased, which was consistent with the expression pattern in intestinal tissues. In addition, we silenced the gene by shRNA interfering and found that the copy numbers of PEDV were remarkably increased in the gene silencing cells. Our findings suggest that the gene was potentially involved in regulating PEDV infection and in maintaining the integrity of the intestinal mucosal barrier structure, which could contribute to our understanding of the mechanisms of PEDV pathogenesis and provide a theoretical basis for the identification and application of resistant genes in pig selective breeding for porcine epidemic diarrhea.
猪流行性腹泻病毒(PEDV)感染肠道上皮细胞,破坏肠道黏膜屏障,进而导致仔猪腹泻。胰高血糖素样肽-2(GLP-2)是一种特异性的肠道生长激素,可促进受损肠道黏膜的修复并改善肠道屏障。在本研究中,我们调查了猪[基因名称]基因在调节PEDV感染中的功能。首先确认并收集了因PEDV感染导致肠道结构受损的肠道组织。表达分析表明,[基因名称]基因在十二指肠、空肠和回肠组织中表达,且在肠道黏膜受损的仔猪空肠和回肠中mRNA水平显著下调。体外将PEDV感染猪小肠上皮细胞显示,[基因名称]基因显著降低,这与肠道组织中的表达模式一致。此外,我们通过shRNA干扰使[基因名称]基因沉默,发现该基因沉默细胞中PEDV的拷贝数显著增加。我们的研究结果表明,[基因名称]基因可能参与调节PEDV感染并维持肠道黏膜屏障结构的完整性,这有助于我们理解PEDV发病机制,并为猪流行性腹泻抗性基因在猪选择性育种中的鉴定和应用提供理论依据。