Histone deacetylase SIR2 in Toxoplasma gondii modulates functions of murine macrophages in vitro and protects mice against acute toxoplasmosis in vivo

文献类型： 外文期刊

第一作者： Yu, ZhengQing

作者： Yu, ZhengQing;Chen, SiYing;Aleem, MuhammadTahir;He, SuHui;Yang, Yang;Zhou, TianYuan;Yan, RuoFeng;Xu, LiXin;Song, XiaoKai;Li, XiangRui;Liu, JunLong;Luo, JianXun

作者机构：

关键词： Toxoplasma gondii; Histone deacetylase; Silent information regulator 2 (SIR2); Murine macrophage; Protective immunity

期刊名称：MICROBIAL PATHOGENESIS （ 影响因子：3.738； 五年影响因子：3.664 ）

ISSN： 0882-4010

年卷期： 2021 年 154 卷

页码：

收录情况： SCI

摘要： Silent information regulator 2 (SIR2) in histone deacetylase (HDAC) is particularly conserved and widely expressed in all eukaryotic cells. HDAC is a crucial post-translational modification protein regulating gene expression. In the present study, a Toxoplasma gondii (T. gondii) silent information regulator 2 (TgSIR2) gene in HDAC was cloned and the modulation effects of recombinant TgSIR2 (rTgSIR2) on murine Ana-1 macrophages were characterized in vitro. The results indicated that rTgSIR2 had a good capacity to eliminate T. gondii by promoting proliferation, apoptosis, and phagocytosis, and modulating the secretion of nitric oxide (NO), proinflammatory cytokines, and anti-inflammatory cytokines. In in vivo experiments, animals were immunized with recombinant TgSIR2, followed by a lethal dose of T. gondii RH strain challenge 14 days after the second immunization. As compared to the blank and control group, the animals immunized with rTgSIR2 could generate specific humoral responses, as demonstrated by the significantly high titers of total IgG and subclasses IgG1 and IgG2a. Significant increases of IFN-gamma, IL-4, and IL-10 were seen, while no significant changes were detected in IL17. The percentage of CD4+ and CD8+ T lymphocytes in animals immunized with rTgSIR2 significantly increased. A significantly long survival time was also observed in animals vaccinated with rTgSIR2 14 days after the last immunization. All these results clearly indicate that rTgSIR2 played an essential role in modulating host macrophages and offered the potential to develop a therapeutic strategy against T. gondii.

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