Coinfection with PCV2 and SS2 enhances the survival of SS2 in swine tracheal epithelial cells by decreasing reactive oxygen species production
Coinfection with PCV2 and SS2 enhances the survival of SS2 in swine tracheal epithelial cells by decreasing reactive oxygen species production
复制标题
猪圆环病毒 2 型 (PCV2) 和猪链球菌血清型 2 (SS2) 的共感染可通过减少活性氧的产生来增强 SS2 在猪气管上皮细胞中的存活率。
DOI：
10.1128/iai.00537-20
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发表时间：
2020
影响因子：
3.1
通讯作者：
Xiaomin Wang
中科院分区：
文献类型：
--
作者：
Qing Wang;Hong Zhou;Hongjie Fan;Xiaomin Wang
猪圆环病毒2型（PCV 2）和猪链球菌血清2型（SS 2）临床合并感染病例频繁发现。呼吸道上皮在宿主防御各种吸入性病原体中起着至关重要的作用。活性氧（Reactive oxygen species，ROS）参与机体对细菌的杀伤和免疫应答。本研究的目的是评估PCV 2和SS 2共感染猪气管上皮细胞（STEC）是否影响ROS的产生，并研究ROS在细菌存活和炎症反应中的作用。与SS 2感染相比，PCV 2/SS 2共感染抑制了NADPH氧化酶的活性，导致ROS水平降低。细菌细胞内存活实验表明，PCV 2和SS 2的共感染增强了SS 2在STEC中的存活。用N-乙酰半胱氨酸（NAC）预处理STEC也有助于SS 2的细胞内存活，这表明PCV 2/SS 2共感染通过减少活性氧产生来增强SS 2在STEC中的存活。此外，与SS 2感染的STEC相比，PCV 2/SS 2共感染和在SS 2感染前用NAC预处理STEC均下调炎性细胞因子白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）和IL-1β的表达。进一步的研究发现，p38/MAPK的激活促进了SS 2感染的STEC中炎性细胞因子的表达;然而，PCV 2/SS 2共感染或STEC的NAC预处理抑制了p38磷酸化，这表明STEC与PCV 2和SS 2共感染通过减少ROS产生来减弱对SS 2感染的炎症反应。总的来说，STEC与PCV 2和SS 2的共感染增强了SS 2的细胞内存活，并通过减少ROS产生来减弱炎症反应，这可能加剧宿主中的SS 2感染。
Porcine circovirus type 2 (PCV2) and Streptococcus suis serotype 2 (SS2) clinical coinfection cases have been frequently detected. The respiratory epithelium plays a crucial role in host defense against a variety of inhaled pathogens. Reactive oxygen species (ROS) are involved in killing of bacteria and host immune response. The aim of this study is to assess whether PCV2 and SS2 coinfection in swine tracheal epithelial cells (STEC) affects ROS production and investigate the roles of ROS in bacterial survival and the inflammatory response. Compared to SS2 infection, PCV2/SS2 coinfection inhibited the activity of NADPH oxidase, resulting in lower ROS levels. Bacterial intracellular survival experiments showed that coinfection with PCV2 and SS2 enhanced SS2 survival in STEC. Pretreatment of STEC with N-acetylcysteine (NAC) also helps SS2 intracellular survival, indicating that PCV2/SS2 coinfection enhances the survival of SS2 in STEC through a decrease in ROS production. In addition, compared to SS2-infected STEC, PCV2/SS2 coinfection and pretreatment of STEC with NAC prior to SS2 infection both downregulated the expression of the inflammatory cytokines interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and IL-1β. Further research found that activation of p38/MAPK promoted the expression of inflammatory cytokines in SS2-infected STEC; however, PCV2/SS2 coinfection or NAC pretreatment of STEC inhibited p38 phosphorylation, suggesting that coinfection of STEC with PCV2 and SS2 weakens the inflammatory response to SS2 infection through reduced ROS production. Collectively, coinfection of STEC with PCV2 and SS2 enhances the intracellular survival of SS2 and weakens the inflammatory response through decreased ROS production, which might exacerbate SS2 infection in the host.