Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5545252 | Veterinary Microbiology | 2017 | 8 Pages |
Abstract
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.
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Authors
Jiangnan Li, Shengnan Wang, Changyao Li, Chunlai Wang, Yonggang Liu, Gang Wang, Xijun He, Liang Hu, Yuanyuan Liu, Mengmeng Cui, Caihong Bi, Zengyu Shao, Xiaojie Wang, Tao Xiong, Xuehui Cai, Li Huang, Changjiang Weng,