Transmissible gastroenteritis virus and porcine epidemic diarrhoea virus infection induces dramatic changes in the tight junctions and microfilaments of polarized IPEC-J2 cells.
Transmissible gastroenteritis virus and porcine epidemic diarrhoea virus infection induces dramatic changes in the tight junctions and microfilaments of polarized IPEC-J2 cells.
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传染性胃肠炎病毒和猪流行性腹泻病毒感染引起极化IPEC-J2细胞紧密连接和微丝的巨大变化
DOI：
10.1016/j.virusres.2014.08.014
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发表时间：
2014-11-04
期刊：
影响因子：
5
通讯作者：
Yang Q
中科院分区：
文献类型：
--
作者：
Zhao S;Gao J;Zhu L;Yang Q
我们检测了PEDV和TGEV在肠模型细胞（IPEC-J2细胞）中的感染。两种病毒在感染的早期阶段损害IPEC-J2细胞。PEDV和TGEV感染影响IPEC-J2细胞的微丝重构。药物干扰的IPEC-J2细胞微丝抑制两个病毒生命周期。MAPKs影响两种病毒感染的IPEC-J2细胞的AJ和微丝。病毒感染改变细胞的正常结构以优化病毒进入、复制和病毒体产生。利用猪流行性腹泻病毒（PEDV）、猪传染性胃肠炎病毒（TGEV）和正常肠上皮细胞模型（IPEC-J2），研究了猪流行性腹泻病毒（PEDV）、猪传染性胃肠炎病毒（TGEV）对猪肠道上皮细胞的致病作用，并对猪肠道上皮细胞的致病机理进行了初步探讨。我们研究了IPEC-J2细胞的紧密连接、粘附连接和微丝与这些病毒的相互作用。结果表明，IPEC-J2细胞对TGEV和PEDV感染敏感。TGEV可通过下调细胞紧密连接和粘附连接蛋白的表达，在感染的早期损害IPEC-J2细胞屏障的完整性，而PEDV云则对上皮屏障的完整性造成轻微损害。此外，它们还可以影响IPEC-J2细胞的微丝重构，药物干预的微丝可以抑制病毒的复制和释放。PEDV + TGEV联合感染比单独感染更能加重细胞间紧密连接的破坏和微丝的重构。最后，PEDV和TGEV感染影响MAPK通路，MAPK通路的抑制调节细胞紧密连接和微丝的变化。这些研究从上皮屏障和微丝的角度为PEDV和TGEV的发病机制提供了新的见解。
We examine infection of PEDV and TGEV in intestinal model cells (IPEC-J2 cells). Two viruses impair of IPEC-J2 cells in their early stages of infection. PEDV and TGEV infection affect the microfilaments remodelling of IPEC-J2 cells. Drug-interfered microfilaments of IPEC-J2 cells inhibit two viral life cycles. MAPKs affected two viruses infection, the AJ and microfilaments of IPEC-J2 cells. Viral infection converts the normal constitution of a cell to optimise viral entry, replication, and virion production. These conversions contain alterations or disruptions of the tight and adherens junctions between cells as part of their pathogenesis, and reorganise cellular microfilaments that initiate, sustain and spread the viral infections and so on. Using porcine epidemic diarrhoea virus (PEDV), transmissible gastroenteritis virus (TGEV) and a model of normal intestinal epithelial cells (IPEC-J2), we researched the interaction between tight and adherens junctions and microfilaments of IPEC-J2 cells with these viruses. In our work, the results showed that IPEC-J2 cells were susceptible to TGEV and PEDV infection. And TGEV could impair the barrier integrity of IPEC-J2 cells at early stages of infection through down-regulating some proteins of tight and adherens junctions, while PEDV cloud cause a slight of damage in the integrity of epithelial barrier. In addition, they also could affect the microfilaments remodelling of IPEC-J2 cells, and the drug-interfered microfilaments could inhibit viral replication and release. Furthermore, PEDV + TGEV co-infection was more aggravating to damage of tight junctions and remodelling of microfilaments than their single infection. Finally, the PEDV and TGEV infection affected the MAPK pathway, and inhibition of MAPK pathway regulated the changes of tight junctions and microfilaments of cells. These studies provide a new insight from the perspective of the epithelial barrier and microfilaments into the pathogenesis of PEDV and TGEV.
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DOI：
10.3390/v3020102
发表时间：
2011-02
期刊：
Viruses
影响因子：
--
作者：
Avota E;Gassert E;Schneider-Schaulies S
通讯作者：
Schneider-Schaulies S
影响因子：
5.5
作者：
Kutsuna, H;Suzuki, K;Kitagawa, S
通讯作者：
Kitagawa, S
影响因子：
2.2
作者：
Liu, Fangning;Li, Guohua;Yuan, Lijuan
通讯作者：
Yuan, Lijuan
影响因子：
4.8
作者：
Gerits, Nancy;Mikalsen, Theresa;Moens, Ugo
通讯作者：
Moens, Ugo
影响因子：
4.8
作者：
Guglielmi, Kristen M.;Kirchner, Eva;Dermody, Terence S.
通讯作者：
Dermody, Terence S.