Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1281827 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR34169825.fastq.gz | Fastqsanger.gz | |||
| SRR34169828.fastq.gz | Fastqsanger.gz | |||
| SRR34169829.fastq.gz | Fastqsanger.gz | |||
| SRR34169831.fastq.gz | Fastqsanger.gz |
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Project description:Porcine epidemic diarrhea virus (PEDV) has reemerged as the main pathogen of piglets due to its high mutation feature. Monolaurin (ML) is a natural compound with a wide range of antibacterial and antiviral activities. However, the role of ML in PEDV infection is still unknown. This study aimed to evaluate the effect of ML on the growth performance, intestinal function, virus replication and cytokine response in piglets infected with PEDV, and to reveal the mechanism through proteomics analysis. Piglets were orally administrated with ML at a dose of 100 mg/kg·BW for 7 days before PEDV infection. Results showed that although there was no significant effect on the growth performance of piglets, ML administration alleviated the diarrhea caused by PEDV infection. ML administration promoted the recovery of intestinal villi, thereby improving intestinal function. Meanwhile, PEDV replication was significantly inhibited, and PEDV-induced expression of IL-6 and IL-8 were decreased with ML administration. Proteomics analyses showed that 38 proteins were differentially expressed between PEDV and ML+PEDV groups, and were significantly enriched in the interferon-related pathways. This suggests ML could promote the restoration of homeostasis by regulating the interferon pathway. Overall, the present study demonstrated ML could confer a protective effect against PEDV infection in piglets, and may be developed as a drug or feed additive to prevent and control PEDV disease.
2022-02-16 | PXD029561 | Pride
Project description:Porcine epidemic diarrhea virus (PEDV) causes severe intestinal damage and high mortality in neonatal piglets. The continuous emergence of new strains has brought new challenges to prevention and control. In this study, we isolated and characterized a prevalent PEDV virulent strain, and analyzed 19,612 jejunal cells from PEDV-infected and control piglets using single-cell sequencing, revealing significant changes in cellular composition, gene expression, and intercellular communication. In response to PEDV infection, epithelial repair was enhanced through increased proliferation and differentiation of stem cells, transit-amplifying (TA) cells, and intestinal progenitor cells into enterocytes. Additionally, PEDV disrupted intercellular communication, compromising epithelial functionality while triggering immune responses, with IFN-II and IL-10 signaling activation acting as critical regulators of immune balance and tissue homeostasis. Beyond enterocytes, viral genes were detected in various other cell types. Further experiments confirmed that PEDV could initiate replication in B and T lymphocytes but was unable to produce infectious progeny, with T cells additionally undergoing virus-induced apoptosis. These findings provide new insights into PEDV tropism, immune evasion, and epithelial repair, revealing complex host-pathogen interactions that shape disease progression and tissue regeneration, thereby contributing to a better understanding of enteric coronavirus pathogenesis.
2025-04-22 | GSE293713 | GEO
Project description:Porcine epidemic diarrhea virus (PEDV) is a highly pathogenic virus that causes severe gastrointestinal disease in neonatal piglets, often leading to high mortality. To advance the study of viral pathogenesis, it is essential to develop an in vitro model that accurately replicates swine enteric coronavirus infections. In this study, we designed a porcine intestinal apical-out organoid culture system that supports viral replication while allowing for long-term culture and experimental manipulation. Using apical-out organoids derived from the duodenum, jejunum, and ileum, we examined region-specific gene expression profiles in response to PEDV infection. Bulk RNA sequencing revealed distinct gene expression patterns, highlighting the regional differences in intestinal physiology during infection. Differential gene expression analysis indicated that each intestinal segment activates specific signaling pathways related to cell survival and antiviral responses following PEDV infection. Functional analyses identified key pathways involved in cell development, signaling, apoptosis, and survival. This study elucidates the mechanisms underlying the differential responses of specific intestinal regions to PEDV, which may inform the selection of optimal models for future PEDV research. In summary, our systematic investigation into the responses of various small intestine segments following PEDV infection provides deeper insights into viral pathogenesis.
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Project description:The immune system is thought to be fragile in the neonate, which is susceptible to pathogens. Exosomes are a type of vehicles existing in the body fluid and participate in many biological processes, especially the immune response. Inorder to investigate the roles that exosomes may play during virus infection in the neonate, porcine epidemic diarrhea virus (PEDV), a devastating enteric virus to newborn piglets, was selected for infection. Serum exosomes were then isolated from the newborn-piglets infected or mock-infected with PEDV and followed by a label-free LC-MS/MS based comparative quantitative proteomic analysis. Among 441 proteins detected in the serum exosomes, there were lots of complement proteins. The expression level of the complement C3, C6 and CFB suffered drastic changes due to PEDV infection. After the confirmation by western-blot assay, we then investigated the function of these exosomes on PEDV infection and discovered that the exosomes from mock-infected newborn piglets restricted PEDV infection but this inhibition disappeared after exosomes were heat-inactivated, suggesting that the complement is one of the key antiviral molecules. These findings will facilitate the understanding of the antiviral response of the neonate mediated by exosomes
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Project description:Swine coronavirus-porcine epidemic diarrhea virus (PEDV) with specific susceptibility to pigs has existed for decades, and recurrent epidemics caused by mutant strains have swept the world again since 2010. Here, single-cell RNA-sequencing was used to perform a systematic analysis of pig small intestines infected with PEDV for the first time. Multiple cell types were identified by representative markers, including the unique marker DNAH11 of tuft cells. Meanwhile, the goblet and tuft cells were also susceptible to PEDV except enterocytes. PEDV infection obviously upregulated REG3G, which significantly inhibited virus replication. Notably, IFN-DELTAs in goblet and enterocyte progenitor cells were increased in virus infected piglet, and IFN-DELTA5 could induce GBP1, ISG15, OAS2 and IFITM1 dramatically raised in IPEC-J2 cells and restricted PEDV replication. Complement molecules were mainly expressed in intestinal cells excepting tuft cells, but PEDV decreased C3, C4A, and C5 in enterocytes, thus escaping the antiviral effect of C3. Finally, enterocytes expressed almost all coronavirus entry factors, and PEDV infection caused significant upregulation of the coronavirus receptor ACE2 in porcine enterocyte cells. In summary, this study systematically studied the response of different cell types in small intestine of pigs after PEDV infection, which deepened the understanding of viral pathogenesis.
2022-04-27 | GSE175411 | GEO
Project description:Emerging knowledge shows the importance of early life events in programming the intestinal mucosal immune system and development of the intestinal barrier function. These processes depend heavily on close interactions between gut microbiota and host cells in the intestinal mucosa. In turn, development of the intestinal microbiota is largely dependent on available nutrients and substrates required for the specific microbial community structures to expand. It is currently not known what the specificities are of intestinal microbial community structures in relation to the programming of the intestinal mucosal immune system and development of the intestinal barrier function. The objective of the present study was to investigate the effect of a nutritional intervention on intestinal development of suckling piglets by daily oral administration of fructooligosaccharides (FOS) over a period of 12 days. At the microbiota community level a clear “bifidogenic” effect of the FOS administration was observed in colon digesta at day 14. The former, however, did not translate into significant changes of local gene expression in the colonic mucosa. In the jejunum, significant changes were observed for microbiota composition at day 14, and microbiota diversity at day 25. In addition, significant differentially expressed gene sets in mucosal tissues of jejunum were identified at both days 14 and 25 of age. At the age of 14 days, lower activity of cell cycle-related processes and a higher activity of extracellular matrix processes were observed in jejunal scrapings of piglets supplemented with FOS compared to control piglets. At day 25, lower activity of immune-related processes in jejunal tissue were seen in piglets supplemented with FOS. Histological parameters, villi height and crypt depth, were significantly different at day 25 between the experimental and control group, where piglets supplemented with FOS had higher villi and deeper crypts. We conclude that oral FOS administration during the suckling period of piglets has significant bifidogenic effects on the microbiota in the colon and on gene expression in jejunal mucosa scrapings. We hypothesize that FOS supplementation of suckling piglets results in a higher butyrate production in the colon due to the increase in bifidobacteria and lactobacilli in the hindgut. We further speculate that a higher butyrate production in colonic digesta relates to changes in gene expression in the jejunum by thus far unknown mechanisms.
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