Poly (I: C) inhibits reticuloendothelial virus replication in chicken macrophage-like cells through the activation of toll-like receptor-3 signaling
Autor: | Yu Bai, Chaonan Liu, Xinhua Cui, Xiaoping Lv, Shimin Zheng, Xueli Gao |
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Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
Interferon Inducers Immunology Reticuloendotheliosis Viruses Avian Virus Replication Antiviral Agents Virus Cell Line 03 medical and health sciences 0302 clinical medicine Interferon medicine Animals Secretion Molecular Biology Messenger RNA Toll-like receptor Chemistry Macrophages Interferon-beta Mononuclear phagocyte system Molecular biology Toll-Like Receptor 3 Tumor Virus Infections Poly I-C 030104 developmental biology Viral replication Cell culture Chickens Retroviridae Infections Signal Transduction 030215 immunology medicine.drug |
Zdroj: | Molecular Immunology. 136:110-117 |
ISSN: | 0161-5890 |
DOI: | 10.1016/j.molimm.2021.05.013 |
Popis: | Reticuloendothelial virus (REV) is widely found in many domestic poultry areas and results in severe immunosuppression of infected chickens. This increases the susceptibility to other pathogens, which causes economic losses to the poultry industry. The aim of our study was to determine whether polyinosinic-polycytidylic acid [Poly (I: C)] treatment could inhibit REV replication in chicken macrophage-like cell line, HD11. We found that Poly (I: C) treatment could markedly inhibit REV replication in HD11 from 24 to 48 h post infection (hpi). Additionally, Poly (I: C) treatment could switch HD11 from an inactive type into M1-like polarization from 24 to 48 hpi. Furthermore, Poly (I: C) treatment promoted interferon-β secretion from HD11 post REV infection. Moreover, Toll-like receptor-3 (TLR-3) mRNA and protein levels in HD11 treated with Poly (I: C) were markedly increased compared to those of HD11 not treated with Poly (I: C). The above results suggested that Poly (I: C) treatment switches HD11 into M1-like polarization to secret more interferon-β and activate TLR-3 signaling, which contributes to block REV replication. Our findings provide a theoretical reference for further studying the underlying pathogenic mechanism of REV and Poly (I: C) as a potential therapeutic intervention against REV infection. |
Databáze: | OpenAIRE |
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