Dataset Information

Lack of LT?R Increases Susceptibility of IPEC-J2 Cells to Porcine Epidemic Diarrhea Virus.

ABSTRACT: The essential requirement of the lymphotoxin beta receptor (LT?R) in the development and maintenance of peripheral lymphoid organs is well recognized. Evidence shows that LT?R is involved in various cellular processes; however, whether it plays a role in maintaining the cellular function of intestinal porcine enterocytes (IPEC-J2), specifically during porcine epidemic diarrhea virus (PEDV) infection, remains unknown. In this study, we generated LT?R null IPEC-J2 cells using CRISPR/Cas9 to examine the importance of LT?R in cell proliferation, apoptosis, and the response to PEDV infection. Our results showed that the lack of LT?R leads to significantly decreased cell proliferation, potentially due to S phase arrest in LT?R^-/- IPEC-J2 cells. Label-free digital holographic microscopy was used to record the three-dimensional morphology of both cell types for up to 72 hours and revealed significantly increased numbers of LT?R^-/- cells undergoing apoptosis. Furthermore, we found that PEDV-infected LT?R^-/- null IPEC-J2 cells exhibited significant suppression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF?B) target genes (interleukin (IL)-6 and IL-8) and mucosal barrier integrity-related genes (vascular cell adhesion molecule 1 (VCAM1) and IL-22), which may explain why LT?R^-/- cells are more susceptible to PEDV infection. Collectively, our data not only demonstrate the key role of LT?R in intestinal porcine enterocytes, but also provide data for the improved understanding of the cellular response to PEDV infection.

SUBMITTER: Altawaty T

PROVIDER: S-EPMC6262443 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Lack of LTβR Increases Susceptibility of IPEC-J2 Cells to Porcine Epidemic Diarrhea Virus.

Altawaty Tawfeek T Liu Lulu L Zhang Hongyong H Tao Cong C Hou Shaohua S Li Kui K Wang Yanfang Y

Cells 20181121 11

The essential requirement of the lymphotoxin beta receptor (LTβR) in the development and maintenance of peripheral lymphoid organs is well recognized. Evidence shows that LTβR is involved in various cellular processes; however, whether it plays a role in maintaining the cellular function of intestinal porcine enterocytes (IPEC-J2), specifically during porcine epidemic diarrhea virus (PEDV) infection, remains unknown. In this study, we generated LTβR null IPEC-J2 cells using CRISPR/Cas9 to examin ...[more]

PMID: 30469426

Similar Datasets

Project description:Porcine epidemic diarrhea virus (PEDV) infection causes watery diarrhea and vomiting in piglets. The pathogenesis of PEDV infection is related to intestinal inflammation. It is known that 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) has potent anti-inflammatory activity, but it is unknown whether 1,25(OH)2D3 can inhibit the PEDV-induced inflammatory response and the underlying mechanism. We used transcriptome analysis, gene and protein expression, RNA interference and overexpression, and other techniques to study the anti-inflammatory effects of 1,25(OH)2D3 on PEDV infection in IPEC-J2 cells. The results showed that interleukin 19 (IL-19) and C-C motif chemokine ligand 20 (CCL20) gene expression were enhanced with the increase in PEDV infection time in IPEC-J2 cells. Interestingly, 1,25(OH)2D3 supplementation obviously inhibited IL-19 and CCL20 expression induced by PEDV. Meanwhile, we also found that 1,25(OH)2D3 reduced p-NF-κB, p-STAT1, and p-STAT3 protein levels induced by PEDV at 24 h post-infection. IκBα and SOCS3, NF-κB, and STAT inhibitor respectively, were increased by 1,25(OH)2D3 supplementation upon PEDV infection. In addition, 1,25(OH)2D3 supplementation inhibited ISG15 and MxA expression induced by PEDV. Although 1,25(OH)2D3 suppressed the JAK/STAT signal pathway and antiviral gene expression, it had no significant effects on PEDV replication and IFN-α-induced antiviral effects. In addition, when the vitamin D receptor (VDR) was silenced by siRNA, the anti-inflammatory effect of 1,25(OH)2D3 was inhibited. Meanwhile, the overexpression of VDR significantly downregulated IL-19 and CCL20 expression induced by PEDV infection. Together, our results provide powerful evidence that 1,25(OH)2D3 could alleviate PEDV-induced inflammation by regulating the NF-κB and JAK/STAT signaling pathways through VDR. These results suggest that vitamin D could contribute to inhibiting intestinal inflammation and alleviating intestinal damage in PEDV-infected piglets, which offers new approaches for the development of nutritional strategies to prevent PEDV infection in piglets.

Dataset Information

Lack of LT?R Increases Susceptibility of IPEC-J2 Cells to Porcine Epidemic Diarrhea Virus.

Publications

Lack of LTβR Increases Susceptibility of IPEC-J2 Cells to Porcine Epidemic Diarrhea Virus.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets