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.

中文翻译：

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猪圆环病毒2型利用JNK介导的紧密连接破坏来促进猪链球菌跨气管上皮转运。

猪圆环病毒2型（PCV2）被认为是猪圆环病毒相关疾病（PCVAD）的主要病原体，在世界范围内造成了巨大的经济损失。临床上，PCV2通常通过与其他细菌性病原体（包括猪链球菌（S. suis），尤其是高度流行的猪链球菌2型（SS2））共感染而引起疾病。本研究确定了仔猪的连续PCV2感染下调了肺中的紧密连接蛋白（TJ）ZO-1和occludin。用猪气管上皮细胞（STEC）探索破坏TJ的机制和后果，并建立了体外气管上皮屏障模型。我们的结果表明，STEC中PCV2感染会降低ZO-1和occludin的表达水平，并增加气管上皮屏障的通透性，导致SS2易位。此外，蛋白质印迹分析表明PCV2感染激活JNK / MAPK途径。抑制JNK磷酸化可以减轻PCV2诱导的SETC中TJ的破坏和上皮屏障通透性的增加，这表明JNK / MAPK途径在PCV2感染期间调节ZO-1和occludin的表达。这项研究使我们能够更好地了解PCV2与细菌病原体共感染的机制，并为控制PCVAD的发生提供新的见解。抑制JNK磷酸化可以减轻PCV2诱导的SETC中TJ的破坏和上皮屏障通透性的增加，这表明JNK / MAPK途径在PCV2感染期间调节ZO-1和occludin的表达。这项研究使我们能够更好地了解PCV2与细菌病原体共感染的机制，并为控制PCVAD的发生提供新的见解。抑制JNK磷酸化可以减轻PCV2诱导的SETC中TJ的破坏和上皮屏障通透性的增加，这表明JNK / MAPK途径在PCV2感染期间调节ZO-1和occludin的表达。这项研究使我们能够更好地了解PCV2与细菌病原体共感染的机制，并为控制PCVAD的发生提供新的见解。