Diarrhea, caused by porcine epidemic diarrhea virus (PEDV), is a catastrophic gastrointestinal disease among suckling piglets, with high infectivity, morbidity, and mortality, causing huge economic losses to the pig industry. In the present study, we investigated the different microbiota from the cecal mucosa and cecal contents between healthy and PEDV-infected piglets. High-throughput 16S rRNA gene sequencing was performed to explore differences. The results revealed that microbial dysbiosis by PEDV infection occurred in the cecal mucosa and contents of suckling piglets at each microbial taxonomic level. The abundance of pathogenic bacteria associated with diseases, including diarrhea, was increased. The abundance of Fusobacterium was 26.71% and 33.91% in cecal mucosa and contents of PEDV-infected group, respectively, whereas that in the healthy groups was 17.85% and 9.88%. The proportion of Proteobacteria in the infected groups was relatively high (24.67% and 22.79%, respectively), whereas that in the healthy group was 13.13% and 11.34% in the cecal mucosa and contents, respectively. Additionally, the proportion of Bacteroidetes in the healthy group (29.89%, 37.32%) was approximately twice that of the PEDV-infected group (15.50%, 15.39%). “Nitrate reduction”, “Human pathogens diarrhea”, “Human pathogens gastroenteritis”, “Nitrite respiration”, and “Nitrite ammonification” were the enriched functional annotation terms in the PEDV-infected groups. Porcine epidemic diarrhea virus infection increased the proportion of harmful bacteria and decreased the proportion of beneficial bacteria in the cecal mucosa and contents of suckling piglets. Our findings suggest that determining the intestinal microbiota might provide a promising method to prevent PEDV and open a new avenue for future research.
Porcine epidemic diarrhea (PED) is a major gastrointestinal disease afflicting suckling pigs that causes huge industrial economic losses. In this study, we investigated microbiota from the colonic mucosa and content in healthy and PED piglets. High-throughput 16S rRNA gene sequencing was performed to identify inter-group differences. Firmicutes, Fusobacteria, Proteobacteria, and Bacteroidetes were the top four affected phyla. The proportion of Proteobacteria was higher in infected than in healthy piglets, and the opposite was observed for Bacteroidetes (more than four-fold higher in the healthy group). In the infected group, Fusobacterium accounted for 36.56% and 21.61% in the colonic mucosa and contents, respectively, while in the healthy group, they comprised 22.53% and 12.67%, respectively. The percentage of Lactobacillus in healthy colons (15.63%) was considerably higher than that in the disease group (<10%). In both the colonic mucosa and contents, functional enrichment differed significantly between healthy and diseased groups. Overall, infection with the PED virus increased the proportion of harmful bacteria and decreased the proportion of beneficial bacteria in the colons of piglets. Targeting intestinal microbiota could be a promising method for PED prevention, thus opening new avenues for future research.
Epigenetic modification plays a critical role in establishing and maintaining cell differentiation, embryo development, tumorigenesis and many complex diseases. However, little is known about the epigenetic regulatory mechanisms for milk production in dairy cattle. Here, we conducted an epigenome‐wide study, together with gene expression profiles to identify important epigenetic candidate genes related to the milk production traits in dairy cattle. Whole‐genome bisulphite sequencing and RNA sequencing were employed to detect differentially methylated genes (DMG) and differentially expressed genes (DEG) in blood samples in dry period and lactation period between two groups of cows with extremely high and low milk production performance. A total of 10,877 and 6,617 differentially methylated regions were identified between the two groups in the two periods, which corresponded to 3,601 and 2,802 DMGs, respectively. Furthermore, 156 DEGs overlap with DMGs in comparison of the two groups, and 131 DEGs overlap with DMGs in comparison of the two periods. By integrating methylome, transcriptome and GWAS data, some potential candidate genes for milk production traits in dairy cattle were suggested, such as DOCK1, PTK2 and PIK3R1. Our studies may contribute to a better understanding of epigenetic modification on milk production traits of dairy cattle.
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.
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