scholarly journals Identification and analysis of long non-coding RNAs that are involved in inflammatory process in response to transmissible gastroenteritis virus infection

2019 ◽  
Author(s):  
Xuelian Ma ◽  
Xiaomin Zhao ◽  
Kaili Wang ◽  
Xiaoyi Tang ◽  
Jianxiong Guo ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Messenger Rna ◽  
Binding Proteins ◽  
Differentially Expressed ◽  
Transmissible Gastroenteritis Virus ◽  
Intestinal Epithelial ◽  
Antisense Gene ◽  
Gastroenteritis Virus ◽  
Expression Of Genes ◽  
Transmissible Gastroenteritis

Abstract Abstract Background: Transmissible gastroenteritis virus (TGEV) infection can cause acute inflammation. Long noncoding RNAs (lncRNAs) play important roles in a number of biological process including inflammation response. However, whether lncRNAs participate in TGEV-induced inflammation in porcine intestinal epithelial cells (IPECs) is largely unknown. Results: In this study, the next-generation sequencing (NGS) technology was used to analyze the profiles of lncRNAs in Mock and TGEV-infected porcine intestinal epithelial cell-jejunum 2 (IPEC-J2) cell line. A total of 106 lncRNAs were differentially expressed. Many differentially expressed lncRNAs act as elements to competitively attach microRNAs (miRNAs) which target to messenger RNA (mRNAs ) to mediate expression of genes that related to Toll-like receptors (TLRs), NOD-like receptors (NLRs), Tumor necrosis factor (TNF), and RIG-I-like receptor s (RLRs) pathways. Functional analysis of the binding proteins and the up/down-stream genes of the differentially expressed lncRNAs revealed that lncRNAs were principally related to inflammatory response. Meanwhile, we found that the differentially expressed lncRNA TCONS_00058367 might lead to a reduction of phosphorylation of transcription factor p65 (p-p65) in TGEV-infected IPEC-J2 cells by negatively regulating its antisense gene romyelocytic leukemia (PML ). Conclusions: The data showed that differentially expressed lncRNAs might be involved in inflammatory response induced by TGEV through acting as miRNA sponges, regulating their up/down-stream genes, or directly binding proteins.

scholarly journals Identification and analysis of long non-coding RNAs that are involved in inflammatory process in response to transmissible gastroenteritis virus infection

BMC Genomics ◽  
2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Xuelian Ma ◽  
Xiaomin Zhao ◽  
Kaili Wang ◽  
Xiaoyi Tang ◽  
Jianxiong Guo ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Messenger Rna ◽  
Binding Proteins ◽  
Differentially Expressed ◽  
Transmissible Gastroenteritis Virus ◽  
Intestinal Epithelial ◽  
Antisense Gene ◽  
Gastroenteritis Virus ◽  
Expression Of Genes ◽  
Transmissible Gastroenteritis

Abstract Background Transmissible gastroenteritis virus (TGEV) infection can cause acute inflammation. Long noncoding RNAs (lncRNAs) play important roles in a number of biological process including inflammation response. However, whether lncRNAs participate in TGEV-induced inflammation in porcine intestinal epithelial cells (IPECs) is largely unknown. Results In this study, the next-generation sequencing (NGS) technology was used to analyze the profiles of lncRNAs in Mock and TGEV-infected porcine intestinal epithelial cell-jejunum 2 (IPEC-J2) cell line. A total of 106 lncRNAs were differentially expressed. Many differentially expressed lncRNAs act as elements to competitively attach microRNAs (miRNAs) which target to messenger RNA (mRNAs) to mediate expression of genes that related to toll-like receptors (TLRs), NOD-like receptors (NLRs), tumor necrosis factor (TNF), and RIG-I-like receptors (RLRs) pathways. Functional analysis of the binding proteins and the up/down-stream genes of the differentially expressed lncRNAs revealed that lncRNAs were principally related to inflammatory response. Meanwhile, we found that the differentially expressed lncRNA TCONS_00058367 might lead to a reduction of phosphorylation of transcription factor p65 (p-p65) in TGEV-infected IPEC-J2 cells by negatively regulating its antisense gene promyelocytic leukemia (PML). Conclusions The data showed that differentially expressed lncRNAs might be involved in inflammatory response induced by TGEV through acting as miRNA sponges, regulating their up/down-stream genes, or directly binding proteins.

scholarly journals Identification and analysis of long non-coding RNAs that are involved in inflammatory process in response to transmissible gastroenteritis virus infection

2019 ◽  
Author(s):  
Xuelian Ma ◽  
Xiaomin Zhao ◽  
Kaili Wang ◽  
Xiaoyi Tang ◽  
Jianxiong Guo ◽  
...  
Keyword(s):  
Immune Response ◽  
Binding Proteins ◽  
Differentially Expressed ◽  
Transmissible Gastroenteritis Virus ◽  
Intestinal Epithelial ◽  
Antisense Gene ◽  
Gastroenteritis Virus ◽  
Expression Of Genes ◽  
Transmissible Gastroenteritis ◽  
Mirna Sponges

Abstract Abstract Background: Transmissible gastroenteritis virus (TGEV) infection can activate the immune response and cause inflammation. Long noncoding RNAs (lncRNAs) play important roles in antiviral innate immune response. However, whether lncRNAs participate in TGEV-induced inflammation in porcine intestinal epithelial cells (IPECs) is largely unknown. Results: In this study, the next-generation sequencing (NGS) technology was used to analyze the profiles of lncRNAs in Mock and TGEV-infected porcine intestinal epithelial cell-jejunum 2 (IPEC-J2) cell line. A total of 106 lncRNAs were differentially expressed. Many differentially expressed lncRNAs act as elements to competitively attach miRNAs with mRNAs to mediate expression of genes that related to Toll-like receptor, NOD-like receptor, TNF, and RIG-I-like receptor pathways. Functional analysis of the binding proteins and the up/down-stream genes of the differentially expressed lncRNAs revealed that lncRNAs were principally related to immune response. Meanwhile, we found that the differentially expressed lncRNA TCONS_00058367 might lead to a reduction of p-p65 in TGEV-infected IPEC-J2 cells by negatively regulating its antisense gene PML. Conclusions: The data showed that differentially expressed lncRNAs might be involved in immune response induced by TGEV through acting as miRNA sponges, regulating their up/down-stream genes, or directly binding proteins.

scholarly journals Persistent Transmissible Gastroenteritis Virus Infection Enhances Enterotoxigenic Escherichia coli K88 Adhesion by Promoting Epithelial-Mesenchymal Transition in Intestinal Epithelial Cells

2017 ◽  
Vol 91 (21) ◽  
Author(s):  
Lu Xia ◽  
Lei Dai ◽  
Qinghua Yu ◽  
Qian Yang
Keyword(s):  
Epithelial Cells ◽  
Epithelial Mesenchymal Transition ◽  
Secondary Infection ◽  
Dual Infection ◽  
Transmissible Gastroenteritis Virus ◽  
Intestinal Epithelial ◽  
Mesenchymal Transition ◽  
Gastroenteritis Virus ◽  
Integrin Α5 ◽  
Transmissible Gastroenteritis

ABSTRACT Transmissible gastroenteritis virus (TGEV) is a coronavirus characterized by diarrhea and high morbidity rates, and the mortality rate is 100% in piglets less than 2 weeks old. Pigs infected with TGEV often suffer secondary infection by other pathogens, which aggravates the severity of diarrhea, but the mechanisms remain unknown. Here, we hypothesized that persistent TGEV infection stimulates the epithelial-mesenchymal transition (EMT), and thus enterotoxigenic Escherichia coli (ETEC) can more easily adhere to generating cells. Intestinal epithelial cells are the primary targets of TGEV and ETEC infections. We found that TGEV can persistently infect porcine intestinal columnar epithelial cells (IPEC-J2) and cause EMT, consistent with multiple changes in key cell characteristics. Infected cells display fibroblast-like shapes; exhibit increases in levels of mesenchymal markers with a corresponding loss of epithelial markers; have enhanced expression levels of interleukin-1β (IL-1β), IL-6, IL-8, transforming growth factor β (TGF-β), and tumor necrosis factor alpha (TNF-α) mRNAs; and demonstrate increases in migratory and invasive behaviors. Additional experiments showed that the activation of the phosphatidylinositol 3-kinase (PI3K)/Akt and extracellular signal-regulated kinase (ERK) signaling pathways via TGF-β is critical for the TGEV-mediated EMT process. Cellular uptake is also modified in cells that have undergone EMT. TGEV-infected cells have higher levels of integrin α5 and fibronectin and exhibit enhanced ETEC K88 adhesion. Reversal of EMT reduces ETEC K88 adhesion and inhibits the expression of integrin α5 and fibronectin. Overall, these results suggest that TGEV infection induces EMT in IPEC-J2 cells, increasing the adhesion of ETEC K88 in the intestine and facilitating dual infection. IMPORTANCE Transmissible gastroenteritis virus (TGEV) causes pig diarrhea and is often followed by secondary infection by other pathogens. In this study, we showed that persistent TGEV infection induces an EMT in porcine intestinal columnar epithelial cells (IPEC-J2) and enhances the adhesion of the secondary pathogen ETEC K88. Additional experiments suggest that integrin α5 and fibronectin play an important role in TGEV-enhanced ETEC K88 adhesion. Reversal of EMT reduces the expression of integrin α5 and fibronectin and also reduces ETEC K88 adhesion. We conclude that TGEV infection triggers EMT and facilitates dual infection. Our results provide new insights into secondary infection and suggest that targeted anti-EMT therapy may have implications for the prevention and treatment of secondary infection.

scholarly journals Genome-Wide DNA Methylome and Transcriptome Analysis of Porcine Testicular Cells Infected With Transmissible Gastroenteritis Virus

2022 ◽  
Vol 8 ◽  
Author(s):  
Jiayun Wu ◽  
Xiaoru Shi ◽  
Lisi Wu ◽  
Zhengchang Wu ◽  
Shenglong Wu ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Ribosome Biogenesis ◽  
Transmissible Gastroenteritis Virus ◽  
Whole Genome Analysis ◽  
Testicular Cells ◽  
Gastroenteritis Virus ◽  
Expression Of Genes ◽  
Suckling Piglets ◽  
Transmissible Gastroenteritis ◽  
Methylation Patterns

Transmissible gastroenteritis virus (TGEV) is a porcine pathogen causing highly communicable gastrointestinal infection that are lethal for suckling piglets. In an attempt to delineate the pathogenic mechanism of TGEV-infected porcine testicular cells (ST cells), we conducted a whole genome analysis of DNA methylation and expression in ST cells through reduced bisulfate-seq and RNA-seq. We examined alterations in the methylation patterns and recognized 1764 distinct methylation sites. 385 differentially expressed genes (DEGs) were enriched in the viral defense and ribosome biogenesis pathways. Integrative analysis identified two crucial genes (EMILIN2, RIPOR3), these two genes expression were negatively correlated to promoter methylation. In conclusion, alterations in DNA methylation and differential expression of genes reveal that their potential functional interactions in TGEV infection. Our data highlights the epigenetic and transcriptomic landscapes in TGEV-infected ST cells and provides a reliable dataset for screening TGEV resistance genes and genetic markers.

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