中文摘要：

选取8头猪圆环病毒2型（PCV2）和猪繁殖与呼吸综合征病毒（PRRSV）血清抗原、抗体阴性的普通断奶仔猪,无菌取其脾脏制成单细胞悬液后,随机分为4组：对照组、NF-κB抑制剂组（抑制剂组）、PCV2组和NF-κB抑制剂-PCV2组（抑制剂-PCV2组）,体外培养24 h后收获淋巴细胞及培养上清液。ELISA方法检测培养上清液中IL-4和IL-12的含量;间接免疫荧光定位检测PCV2感染淋巴细胞的情况和核因子κB（NF-κB）蛋白入核情况,Western blot定量检测细胞浆中髓样分化因子88（MyD88）、磷酸化抑制性核因子кB（p-IкB）及NF-κB/p65和细胞核中NF-κB/p65蛋白含量的变化,电泳迁移率法（EMSA）检测细胞核中NF-κB与DNA的结合活性。结果显示,细胞培养上清液中,PCV2组IL-4含量明显低于对照组及抑制剂-PCV2组（P〈0.05）,对照组与抑制剂-PCV2组无差异;PCV2组细胞培养上清液中IL-12含量显著高于对照组（P〈0.05）,抑制剂-PCV2组极显著低于PCV2组（P〈0.01）。PCV2感染后可在淋巴细胞内观察到PCV2抗原,并主要存在于细胞浆中。淋巴细胞胞浆内MyD88蛋白含量,PCV2组极显著高于对照组（P〈0.01）,PCV2组与抑制剂-PCV2组之间无显著差异。PCV2组淋巴细胞胞浆内p-IκBα的蛋白含量,胞核中NF-κB/p65含量及NF-κB与DNA结合活性均显著高于对照组;抑制剂和抑制剂-PCV2组淋巴细胞胞浆内p-IκBα的蛋白含量,胞核中NF-κB/p65含量及NF-κB与DNA结合活性均显著低于对照组。结论：PCV2可感染体外培养的仔猪淋巴细胞,介导MyD88-NF-κB信号途径激活从而调节淋巴细胞IL-4和IL-12的分泌。

英文摘要：

Eight post-weaning piglets,which were free of porcine circorirus type 2（PCV2） and porcine reproductive and respiratory syndrome virus（PRRSV）,were chosen as the experimental animals. The suspensions of the single cells isolated from the spleens of these piglets were divided into four groups as follows： control group,nuclear factor kappa B（NF-κB） inhibitor group（inhibitor group）,PCV2 group,and NF-κB inhibitor-PCV2 group（inhibitor-PCV2 group）. After 24 h incubation in vitro,the lymphocytes and the resulting supernatants were harvested respectively. The concentrations of interleukin 12（IL-12） and IL-4 secreted in the supernatants were measured by ELISA. The observation of the PCV2-infected cells and the nuclear translocation of NF-κB were conducted using indirect immunofluorescence assay. The protein concentrations of myeloiddifferentiation factor 88（MyD88）, phosphorylated IкBα（p-IκBα）,NF-κB/p65 in cytoplasm and NF-κB/p65 in nucleus were detected by Western blot. The NF-κBDNA binding activity in nucleus was detected using electrophoretic mobility shift assay（EMSA）. Results as follows： The IL-4 concentration in the PCV2 group was significantly lower than that in the control group as well as in the inhibitor-PCV2 group（P〈 0. 05）,while the IL-4 concentration in the control group was similar to that in the inhibitor-PCV2 group. The IL-12 concentration in the PCV2 group was notably higher than that in the control group（P〈0. 05） as well as in the inhibitor-PCV2 group（P〈0. 01）. After PCV2 infection the lymphocytes,the PCV2 antigens were mostly observed in the lymphocytes cytoplasm. The protein concentration of MyD88 expressed in the lymphocyte cytoplasm in the PCV2 group was markedly higher compared to that in control group（P〈0. 01）,but was similar to that in the inhibitor-PCV2 group. For the PCV2 group,the protein concentrations of p-IκB in the lymphocyte cytoplasm and NF-κB/p65 in the nucleus,and the NF-κB-DNA binding activity were higher than th