Immune response of porcine alveolar macrophages to a concurrent infection with porcine reproductive and respiratory syndrome virus and Haemophilus parasuis in vitro
Language English Country Netherlands Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
26358898
DOI
10.1016/j.vetmic.2015.08.026
PII: S0378-1135(15)30015-8
Knihovny.cz E-resources
- Keywords
- Haemophilus parasuis, IL-1β, PRRSV, Porcine alveolar macrophages, Reactive oxygen species,
- MeSH
- Macrophages, Alveolar immunology microbiology virology MeSH
- Biomarkers analysis MeSH
- Cytokines genetics immunology MeSH
- Haemophilus parasuis immunology MeSH
- Haemophilus Infections complications immunology veterinary virology MeSH
- Coinfection veterinary MeSH
- Cells, Cultured MeSH
- RNA, Messenger metabolism MeSH
- Swine Diseases immunology microbiology virology MeSH
- Swine MeSH
- Gene Expression Regulation, Viral MeSH
- Gene Expression Regulation, Bacterial MeSH
- Porcine Reproductive and Respiratory Syndrome immunology virology MeSH
- Porcine respiratory and reproductive syndrome virus immunology MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Biomarkers MeSH
- Cytokines MeSH
- RNA, Messenger MeSH
Porcine reproductive and respiratory syndrome virus (PRRSV) can predispose pigs to secondary respiratory infection with bacteria such as Haemophilus parasuis. Animals infected with both pathogens develop more severe clinical disease. The immune response of porcine alveolar macrophages (PAMs) to simultaneous infection with PRRSV and H. parasuis was analysed in vitro, describing cytokine production, expression of cell surface molecules, and production of reactive oxygen species (ROS). Concurrent infection with PRRSV and H. parasuis increased gene expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-8) in PAMs in comparison with PAMs infected with PRRSV or H. parasuis alone. An additive effect of dual infection on IL-1β production was confirmed at the protein level. PAMs infected with PRRSV showed increased production of ROS compared to controls. Conversely, simultaneous infection of PAMs with PRRSV and H. parasuis decreased production of ROS, indicating the presence of an H. parasuis defence mechanism against respiratory burst. Concurrent infection of PAMs with PRRSV and H. parasuis was shown to elicit a pro-inflammatory immune response represented by significant IL-1β production. Severe multifactorial respiratory disease in natural conditions caused by both pathogens could be the consequence of pro-inflammatory mediated immunopathology.
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