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Updated: Jul 6, 2025
Isolation, Transfection, and Culture of Primary Human Monocytes
Published on: December 16, 2019
Infection of PRRSV inhibits CSFV C-strain replication by inducing macrophages polarization to M1
Tianbei Tuo1, Dengjin Chen1, Lihong Wang1
1Key Laboratory of Animal Epidemiology of the Ministry of Agriculture, College of Veterinary Medicine, China Agricultural University, Beijing 100193, People's Republic of China.
Abstract:
It is a common sense that porcine reproductive and respiratory syndrome virus (PRRSV) infection could cause immune failure of classical swine fever (CSF) vaccine, and porcine alveolar macrophages (PAMs) are the target cells of both. To elucidate the role of macrophage polarization in PRRSV infection induced CSF vaccine failure, an immortal porcine alveolar macrophage line PAM39 cell line was used to investigate the effect of PRRSV or/and CSFV C-strain (CSFV-C) infection on macrophage polarization in vitro. Interestingly, PRRSV single infection or PRRSV co-infection with CSFV-C promoted PAM39 cells to M1, while CSFV-C single infection induced PAM39 cells to M2. After the construction of M1 and M2 PAM39 cells polarization models, M1 polarized PAM39 cells were found to inhibit the replication of CSFV-C, and Chinese medicine such as matrine, ginsenosides and astragalus polysaccharides could alleviate the polarization of PAM39 cells and the replication of CSFV-C. Furthermore, interferon (IFN)-γ and lipopolysaccharide (LPS) co-stimulation induced NF-κB activation while matrine treatment blocked M1 polarization-induced NF-κB pathway activation. These findings provided a theoretical basis for designing a new strategy to improve the immune effect of CSFV-C based on porcine alveolar macrophage polarization subtypes.
Insights
Porcine reproductive and respiratory syndrome virus (PRRSV) infection impairs classical swine fever (CSF) vaccine efficacy by altering macrophage polarization. M1 macrophages inhibit CSF virus replication, offering a new strategy for vaccine improvement.
Area of Science:
- Immunology
- Virology
- Veterinary Medicine
Background:
- Porcine reproductive and respiratory syndrome virus (PRRSV) infection is known to cause immune failure of classical swine fever (CSF) vaccines.
- Porcine alveolar macrophages (PAMs) are key target cells for both PRRSV and classical swine fever virus (CSFV).
- Macrophage polarization is a critical factor in immune responses and vaccine efficacy.
Purpose of the Study:
- To investigate the role of macrophage polarization in PRRSV-induced CSF vaccine failure.
- To elucidate the effects of PRRSV and CSFV C-strain (CSFV-C) infection on PAM polarization in vitro.
- To explore potential therapeutic strategies for improving CSFV vaccine efficacy.
Main Methods:
- Utilized an immortalized porcine alveolar macrophage cell line (PAM39).
- Infected PAM39 cells with PRRSV and/or CSFV-C to assess macrophage polarization.
- Constructed M1 and M2 PAM39 cell polarization models and evaluated CSFV-C replication.
- Investigated the effects of Chinese medicines (matrine, ginsenosides, astragalus polysaccharides) on PAM polarization and viral replication.
- Analyzed NF-κB pathway activation under different treatment conditions.
Main Results:
- PRRSV single infection or co-infection with CSFV-C promoted M1 polarization of PAM39 cells.
- CSFV-C single infection induced M2 polarization of PAM39 cells.
- M1 polarized PAM39 cells inhibited CSFV-C replication.
- Matrine, ginsenosides, and astragalus polysaccharides alleviated PAM polarization and CSFV-C replication.
- Matrine treatment blocked M1 polarization-induced NF-κB pathway activation.
Conclusions:
- Macrophage polarization plays a significant role in PRRSV-induced CSF vaccine failure.
- M1 macrophage polarization inhibits CSFV-C replication, suggesting a potential therapeutic target.
- Chinese medicines demonstrate potential in modulating macrophage polarization and improving CSFV vaccine efficacy.
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