Analysis of Intestinal Mucosa Integrity and GLP-2 Gene Functions upon Porcine Epidemic Diarrhea Virus Infection in Pigs

Zhou, Yajing; Ren, Zhanshi; Zhang, Shuai; Wang, Haifei; Wu, Shenglong; Bao, Wenbin

SIMPLE SUMMARY: Porcine epidemic diarrhea virus causes serious diarrhea in suckling piglets, resulting in huge economic losses in the pig industry. A better understanding of porcine epidemic diarrhea virus (PEDV) pathogenesis and identification of the responsive genes will contribute to controlling PEDV infection. Therefore, screening and identifying PEDV-resistance functional genes and then implementing disease resistance breeding have important scientific significance. This study explores the regulatory roles of the GLP-2 gene in regulating PEDV infection and in repairing the intestinal mucosa damage associated with PEDV infection. The findings may contribute to the identification of resistant genes or genetic markers for disease resistance breeding in pigs. ABSTRACT: 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 GLP-2 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 GLP-2 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 GLP-2 gene was significantly decreased, which was consistent with the expression pattern in intestinal tissues. In addition, we silenced the GLP-2 gene by shRNA interfering and found that the copy numbers of PEDV were remarkably increased in the GLP-2 gene silencing cells. Our findings suggest that the GLP-2 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.