关键词: 病毒感染, 巨噬细胞, γ-氨基丁酸, 水疱性口炎病毒

Abstract: Objective To investigate the effect and mechanism of metabolite γ-aminobutyric acid (GABA) on viral infection to RAW264.7 cell lines and mouse primary peritoneal macrophages. Methods RAW264.7 cell lines were treated with 0,10,30,50 and 70 mmol/L GABA for 10 hours, and the cellular viability was detected by CCK-8 assay. RAW264.7 cell line was pre-treated with the indicated dose of GABA for 2 hours and then infected with recombinant green fluorescent protein-expressing vesicular stomatitis virus(GFP-VSV) or VSV for 8 hours. The level of GFP-VSV in RAW264.7 cell line was observed by fluorescence microscopy and was detected by flow cytometry. The level of VSV RNA, Ifnb1 and Il-6 mRNA was detected by RT-qPCR. Mouse primary peritoneal macrophages were pre-treated with 0,10, 30, 50 and 70 mmol/L GABA for 2 hours and then infected with VSV for 8 hours. The RNA level of VSV was detected by RT-qPCR. Results It was found that 10,30,50 and 70 mmol/L GABA failed to affect the viability of RAW264.7 cell line. GABA significantly increased the expression of GFP-VSV protein and the level of VSV RNA, Ifnb1 and Il-6 mRNA in RAW264.7 cell line in a dose-dependent manner (all P＜0.05). The level of VSV RNA in mouse primary peritoneal macrophages was also increased in a dose-dependent manner(P＜0.05). Conclusions Metabolite GABA promotes VSV infection to RAW264.7 cell line and mouse primary peritoneal macrophages in a dose-dependent manner, and the mRNA level of Ifnb1 and Il-6 is also increased.

Key words: viral infection, macrophages, γ-aminobutyric acid, vesicular stomatitis virus