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

文献类型： 外文期刊

第一作者： Altawaty, Tawfeek

作者： Altawaty, Tawfeek;Liu, Lulu;Tao, Cong;Hou, Shaohua;Li, Kui;Wang, Yanfang;Liu, Lulu;Zhang, Hongyong

作者机构：

关键词： lymphotoxin beta receptor (LT beta R); intestinal porcine enterocyte cells; CRISPR/Cas9; porcine epidemic diarrhea virus (PEDV) infection

期刊名称：CELLS （ 影响因子：6.6； 五年影响因子：6.663 ）

ISSN： 2073-4409

年卷期： 2018 年 7 卷 11 期

页码：

收录情况： SCI

摘要： The essential requirement of the lymphotoxin beta receptor (LT beta R) in the development and maintenance of peripheral lymphoid organs is well recognized. Evidence shows that LT beta 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 beta R null IPEC-J2 cells using CRISPR/Cas9 to examine the importance of LT beta R in cell proliferation, apoptosis, and the response to PEDV infection. Our results showed that the lack of LT beta R leads to significantly decreased cell proliferation, potentially due to S phase arrest in LT beta 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 beta R-/- cells undergoing apoptosis. Furthermore, we found that PEDV-infected LT beta R-/- null IPEC-J2 cells exhibited significant suppression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF kappa 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 beta R-/- cells are more susceptible to PEDV infection. Collectively, our data not only demonstrate the key role of LTR in intestinal porcine enterocytes, but also provide data for the improved understanding of the cellular response to PEDV infection.

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