Porcine circovirus type 2 exploits JNK-mediated disruption of tight junctions to facilitate Streptococcus suis translocation across the tracheal epithelium
Porcine circovirus type 2 exploits JNK-mediated disruption of tight junctions to facilitate Streptococcus suis translocation across the tracheal epithelium
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2 型猪圆环病毒利用 JNK 介导的紧密连接破坏来促进猪链球菌穿过气管上皮的易位
DOI：
10.1186/s13567-020-00756-2
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发表时间：
2020-02
影响因子：
4.4
通讯作者：
Hongjie Fan
中科院分区：
文献类型：
--
作者：
Qing Wang;Hong Zhou;Huixing Lin;Zhe Ma;Hongjie Fan
猪圆环病毒2型(PCV2)是引起猪圆环病毒相关性疾病(PCVAD)的主要病原，在世界范围内造成巨大的经济损失。在临床上，PCV2常通过与其他细菌性病原体，包括猪链球菌(S.suis)，特别是流行的猪链球菌2型(SS2)的混合感染而致病。本研究确定，仔猪持续感染PCV2可下调肺组织紧密连接蛋白(TJ)、ZO-1和occludin的表达。以猪气管上皮细胞(STEC)为研究对象，探讨TJ破坏的机制和后果，建立体外气管上皮屏障模型。我们的结果表明，PCV2在STEC中的感染降低了ZO-1和occludin的表达水平，并增加了气管上皮屏障的通透性，导致SS2更容易移位。此外，Western印迹分析表明PCV2感染激活了JNK/MAPK通路。抑制JNK的磷酸化可减轻PCV2诱导的SETC细胞TJ的破坏和上皮屏障通透性的增加，提示JNK/MAPK信号通路调节PCV2感染过程中ZO-1和occludin的表达。这项研究有助于我们更好地了解PCV2与细菌病原体混合感染的机制，并为控制PCVAD的发生提供新的视角。
Porcine circovirus type 2 (PCV2) is considered as the primary pathogen of porcine circovirus-associated disease (PCVAD), which results in significant economic losses worldwide. Clinically, PCV2 often causes disease through coinfection with other bacterial pathogens, including Streptococcus suis (S. suis), and especially the highly prevalent S. suis serotype 2 (SS2). The present study determined that continuous PCV2 infection in piglets down-regulates tight junction proteins (TJ) ZO-1 and occludin in the lungs. Swine tracheal epithelial cells (STEC) were used to explore the mechanisms and consequences of disruption of TJ, and an in vitro tracheal epithelial barrier model was established. Our results show that PCV2 infection in STEC decreases the expression levels of ZO-1 and occludin and increases the permeability of the tracheal epithelial barrier, resulting in easier translocation of SS2. Moreover, Western blot analysis indicates that PCV2 infection activates the JNK/MAPK pathway. The disruption of TJ in SETC and increased permeability of the epithelial barrier induced by PCV2 could be alleviated by inhibition of JNK phosphorylation, which indicates that the JNK/MAPK pathway regulates the expression of ZO-1 and occludin during PCV2 infection. This study allows us to better understand the mechanisms of PCV2 coinfection with bacterial pathogens and provides new insight into controlling the occurrence of PCVAD.
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影响因子：
5.3
作者：
通讯作者：
--
影响因子：
4.8
作者：
Lin, Zhijie;Zhang, Yong-Guo;Sun, Jun
通讯作者：
Sun, Jun
影响因子：
30.3
作者：
Drolia R;Tenguria S;Durkes AC;Turner JR;Bhunia AK
通讯作者：
Bhunia AK
影响因子：
--
作者：
Kojima T;Go M;Takano K;Kurose M;Ohkuni T;Koizumi J;Kamekura R;Ogasawara N;Masaki T;Fuchimoto J;Obata K;Hirakawa S;Nomura K;Keira T;Miyata R;Fujii N;Tsutsumi H;Himi T;Sawada N
通讯作者：
Sawada N
DOI：
10.1177/2211068214561025
发表时间：
2015-04
期刊：
Journal of laboratory automation
影响因子：
--
作者：
Srinivasan B;Kolli AR;Esch MB;Abaci HE;Shuler ML;Hickman JJ
通讯作者：
Hickman JJ