Li Jiangnan, Wang Shengnan, Li Changyao, Wang Chunlai, Liu Yonggang, Wang Gang, He Xijun, Hu Liang, Liu Yuanyuan, Cui Mengmeng, Bi Caihong, Shao Zengyu, Wang Xiaojie, Xiong Tao, Cai Xuehui, Huang Li, Weng Changjiang
State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute of Chinese Academy of Agricultural Sciences, Harbin 150069, Heilongjiang, China.
College of Science and Technology, Yangtze University, Jingzhou 434025, Hubei, China.
Vet Microbiol. 2017 May;204:35-42. doi: 10.1016/j.vetmic.2017.03.035. Epub 2017 Apr 8.
Highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) infection often predisposes pigs to secondary bacterial infection, which induces robust inflammatory responses. However, whether the secondary bacterial infection synergizes HP-PRRSV infection and enhances inflammatory responses is not fully understood. Here, we characterized HP-PRRSV infection-mediated secondary bacterial infection and robust inflammatory responses. HP-PRRSV infection induced higher levels of cytokines (IL-1β, IL-18, IL-6 and TNF-α) in the sera in piglets and bacterial loads of 11 bacterial species in the lung were increased after HP-PRRSV infection, including Mycoplasma hyorhinis, Haemophilus parasuis and Escherichia coli. Concurrent infection with HP-PRRSV and H. parasuis model showed that inflammatory cytokines expression and secretion in porcine alveolar macrophages (PAMs) were increased in comparison with PAMs infected with HP-PRRSV or H. parasuis alone. Additionally, we found that H. parasuis RNA plays an important role in the robust inflammatory response enhancement in HP-PRRSV-infected PAMs. Taken together, our findings suggest that bacterial RNA transfection enhanced HP-PRRSV-mediated inflammatory responses in HP-PRRSV and H. parasuis (HPS) concurrent infection, which provides an important clue for comprehensive understanding of HP-PRRSV and bacterial coinfection-mediated pathology.
高致病性猪繁殖与呼吸综合征病毒（HP-PRRSV）感染常使猪易发生继发性细菌感染，从而引发强烈的炎症反应。然而，继发性细菌感染是否会协同HP-PRRSV感染并增强炎症反应，目前尚未完全明确。在此，我们对HP-PRRSV感染介导的继发性细菌感染及强烈的炎症反应进行了特征描述。HP-PRRSV感染导致仔猪血清中细胞因子（IL-1β、IL-18、IL-6和TNF-α）水平升高，且HP-PRRSV感染后肺中11种细菌的载量增加，包括猪鼻支原体、副猪嗜血杆菌和大肠杆菌。HP-PRRSV与副猪嗜血杆菌的共感染模型显示，与单独感染HP-PRRSV或副猪嗜血杆菌的猪肺泡巨噬细胞（PAM）相比，共感染时PAM中炎性细胞因子的表达和分泌增加。此外，我们发现副猪嗜血杆菌RNA在HP-PRRSV感染的PAM中增强强烈炎症反应方面发挥重要作用。综上所述，我们的研究结果表明，在HP-PRRSV与副猪嗜血杆菌（HPS）共感染时，细菌RNA转染增强了HP-PRRSV介导的炎症反应，这为全面理解HP-PRRSV与细菌共感染介导的病理过程提供了重要线索。
