Alterations of Suckling Piglet Jejunal Microbiota Due to Infection With Porcine Epidemic Diarrhea Virus and Protection Against Infection by Lactobacillus salivarius.

Wanting Dong,Zhen Tan,Qin Zhang,Xiangdong Ding,Ning Ding,Yu Zhang,Li Jiang

doi:10.3389/fvets.2021.771411

Abstract

The high mortality of neonatal piglets due to porcine epidemic diarrhea virus (PEDV) infection has caused huge economic losses to the pig industry. The intestinal microbiota is an important barrier against invaders entering the gastrointestinal route. In this study, we examined the differences between intestinal microbiota of PEDV-infected and healthy piglets. According to the viral copy numbers, 16 crossbred (Landrace-Yorkshire) piglets were divided into three groups: uninfected, low virus load, and high virus load groups. Next, 16S rRNA sequencing was performed to determine the microbiota composition in jejunal content and jejunal mucosal samples from the three groups. PEDV infection induced an imbalance in the microbiota of both jejunal content and jejunal mucosa. The abundance of phylum Firmicutes was higher in uninfected piglets than in infected piglets, whereas the abundance of Proteobacteria was lower in uninfected piglets. Principal coordinate analysis showed significant separation of jejunal microbiota between different groups. Linear discriminant analysis (LDA) effect size (LEfSe) identified Lactobacillus salivarius as a potential biomarker among three groups at the level of species. Then, in vitro, L. salivarius was able to suppress the infection of PEDV to IPEC-J2 cells and decreased the expression of GRP78 (Glucose-regulating protein 78). In addition, we detected the mRNA expression of genes involved in the FAK/PI3K/Akt signaling pathway. When IPEC-J2 cells were treated with L. salivarius before PEDV infection, the mRNA expression levels of ITGA1, ITGA5, ITGB5, FAK, PIK3R1, PIK3CA and AKT1 were significantly higher than those in the control cells (without treatment) at different times post-infection, indicating that L. salivarius may upregulate the FAK/PI3K/Akt signaling pathway in IPEC-J2 cells to resist PEDV infection. In summary, PEDV infection altered microbial communities in both jejunal content and jejunal mucosa. L. salivarius has a protective effect against PEDV infection in IPEC-J2 cells. This study provides a potentially effective strategy to prevent the occurrence and control the spread of PED in the pig production.

Highlights

Porcine epidemic diarrhea (PED) is caused by infection with the highly infective porcine epidemic diarrhea virus (PEDV)
As PEDV invades the host via the jejunum, we focused on the jejunal microbiota rather than fecal microbiota
Suckling piglets are most sensitive to PED in the first week of birth [37], and the mortality of PED is close to 100% for newborn piglets and 80% for suckling piglets, resulting in severe losses to the swine industry [38]

Summary

Introduction

Porcine epidemic diarrhea (PED) is caused by infection with the highly infective porcine epidemic diarrhea virus (PEDV). PED is a fatal gastrointestinal disease among suckling piglets that is characterized by high morbidity and mortality. Once infected by PEDV, most sucking piglets suffer severe vomiting and watery diarrhea [1]. The rapid spread of PEDV has caused huge economic losses in the pig industry worldwide. Since 2010, PEDV outbreaks have been widely reported in Asia and North America [2, 3]. Approximately 1,000,000 piglets died from PEDV outbreaks in southern China in the winter of 2010 [4]. In the United States, economic loss attributed to PEDV infection accounted for over 10% of the total losses in the pig industry from 2013 to 2014 [5]. PED has broken out in Canada, Korea, and other countries [6,7,8]

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