Ochratoxin A promotes porcine circovirus type 2 replication in vitro and in vivo.
Ochratoxin A promotes porcine circovirus type 2 replication in vitro and in vivo.
复制标题
赭曲霉毒素 A 可促进猪圆环病毒 2 型体外和体内复制。
DOI：
10.1016/j.freeradbiomed.2014.12.016
复制
发表时间：
2015-03
影响因子：
7.4
通讯作者：
Huang K
中科院分区：
文献类型：
--
作者：
Gan F;Zhang Z;Hu Z;Hesketh J;Xue H;Chen X;Hao S;Huang Y;Cole Ezea P;Parveen F;Huang K
赭曲霉毒素 A (OTA) 是一种世界范围内的真菌毒素，存在于食品和饲料中，对动物和人类来说是一种强效肾毒素。猪圆环病毒相关疾病（PCVAD），包括猪皮炎和肾病综合征，是一种世界性猪病。迄今为止，关于 OTA 与猪圆环病毒 2 型 (PCV2)（PCVAD 的主要病原体）之间的关系知之甚少。在体外和体内研究了 OTA 对 PCV2 复制的影响及其机制。体外结果表明，低剂量的OTA显着增加了PCV2 DNA拷贝数和感染细胞的数量。在 0.05 µg/ml OTA 浓度下观察到最大效果。体内结果表明，与对照组和饲喂150μg/kg OTA的猪相比，饲喂75μg/kg OTA的猪的血清和组织中PCV2复制显着增加。此外，低剂量的 OTA 显着降低了还原型谷胱甘肽以及 NF-E2 相关因子 2 和 γ-谷氨酰半胱氨酸合成酶的 mRNA 表达。活性氧、氧化剂和丙二醛增加；并诱导 PK15 细胞中 p38 和 ERK1/2 磷酸化。添加 N-乙酰基-L-半胱氨酸可逆转 OTA 引起的变化。通过各自的特异性 siRNA 敲低 p38 和 ERK1/2，或通过各自的抑制剂（SB203580 和 U0126）抑制 p38 和 ERK1/2 磷酸化，消除了 OTA 诱导的 PCV2 复制的增加。这些数据表明，低剂量的 OTA 通过氧化应激介导的 p38/ERK1/2 MAPK 信号通路促进 PCV2 在体外和体内的复制。这表明低剂量的 OTA 对动物有潜在危害，因为它们会增强病毒复制，并部分解释了为什么不同猪场的 PCVAD 发病率和严重程度差异很大。
Ochratoxin A (OTA), a worldwide mycotoxin found in food and feeds, is a potent nephrotoxin in animals and humans. Porcine circovirus-associated disease (PCVAD), including porcine dermatitis and nephropathy syndrome, is a worldwide swine disease. To date, little is known concerning the relationship between OTA and porcine circovirus type 2 (PCV2), the primary causative agent of PCVAD. The effects of OTA on PCV2 replication and their mechanisms were investigated in vitro and in vivo. The results in vitro showed that low doses of OTA significantly increased PCV2 DNA copies and the number of infected cells. Maximum effects were observed at 0.05 μg/ml OTA. The results in vivo showed that PCV2 replication was significantly increased in serum and tissues of pigs fed 75 μg/kg OTA compared with the control group and pigs fed 150 μg/kg OTA. In addition, low doses of OTA significantly depleted reduced glutathione and mRNA expression of NF-E2-related factor 2 and γ-glutamylcysteine synthetase; increased reactive oxygen species, oxidants, and malondialdehyde; and induced p38 and ERK1/2 phosphorylation in PK15 cells. Adding N-acetyl-l-cysteine reversed the changes induced by OTA. Knockdown of p38 and ERK1/2 by their respective specific siRNAs or inhibition of p38 and ERK1/2 phosphorylation by their respective inhibitors (SB203580 and U0126) eliminated the increase in PCV2 replication induced by OTA. These data indicate that low doses of OTA promoted PCV2 replication in vitro and in vivo via the oxidative stress-mediated p38/ERK1/2 MAPK signaling pathway. This suggests that low doses of OTA are potentially harmful to animals, as they enhance virus replication, and partly explains why the morbidity and severity of PCVAD vary significantly in different pig farms.
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影响因子：
7.4
作者：
Chen, Xingxiang;Ren, Fei;Huang, Kehe
通讯作者：
Huang, Kehe
DOI：
10.1111/j.1439-0396.2008.00838.x
发表时间：
2009-10-01
影响因子：
2.7
作者：
Boesch-Saadatmandi, C.;Wagner, A. E.;Rimbach, G.
通讯作者：
Rimbach, G.
猪圆环病毒2型复制与体外细胞内氧化还原状态的相互作用
影响因子：
3.8
作者：
Chen, Xingxiang;Ren, Fei;Huang, Kehe
通讯作者：
Huang, Kehe
影响因子：
4.3
作者：
Boesch-Saadatmandi, C.;Loboda, A.;Rimbach, G.
通讯作者：
Rimbach, G.
影响因子：
45.3
作者：
BAILEY, HH;MULCAHY, RT;SPRIGGS, DR
通讯作者：
SPRIGGS, DR