γ干扰素在小鼠生殖道沙眼衣原体感染中的作用机制  被引量:2

M echanism of IFN-γin mice with reproductive tract Chlam ydia trachomatis infection

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作  者:申鑫鑫 豆贝贝 邱红兵 邱文娜 黄向华[2] SHEN Xin-xin;DOU Bei-bei;QIU Hong-bing;QIU Wen-na;HUANG Xiang-hua(Xingtai People's Hos pital,Xingtai,Hebei 054000,China)

机构地区:[1]邢台市人民医院妇科,河北邢台054000 [2]河北医科大学第二附属医院妇科,河北石家庄050000

出  处:《中华医院感染学杂志》2021年第2期171-175,共5页Chinese Journal of Nosocomiology

基  金:河北省医药卫生科技计划基金资助项目(2018MD62)。

摘  要:目的利用鼠衣原体感染小鼠生殖道,探讨γ干扰素(IFN-γ)在小鼠生殖道沙眼衣原体感染中的作用机制。方法通过对小鼠进行鼠衣原体阴道接种得到生殖道感染模型,观察野生型小鼠、IFN-γ基因缺陷小鼠的生存状态,测定体温、体质量、血细胞分类及计数、鼠衣原体(Cm)包涵体计数,观察生殖道组织病理损伤情况,分析外周血中T淋巴细胞亚群水平(CD3^(+)、CD4^(+)、CD8^(+)、CD4^(+)/CD8^(+)),免疫球蛋白(IgG、IgM、IgA)及白细胞介素(IL-1β、IL-17A、IL-12)表达水平。结果小鼠被Cm感染2周后,生存状态差,无干扰基因缺陷组小鼠体温显著高于野生组和注射IFN-γ的基因缺陷组小鼠(P<0.05),体质量低于野生组和注射IFN-γ的基因缺陷组小鼠(P<0.05);无干扰基因缺陷组巨噬细胞水平低于野生组和注射IFN-γ的基因缺陷组(P<0.01);无干扰基因缺陷组Cm包涵体计数最高,野生组次之,注射IFN-γ的基因缺陷组最低(P<0.01),无干扰基因缺陷组外周血中的IL-17A、IgG、IgM水平最低,注射IFN-γ的基因缺陷组的免疫因子水平与野生组接近(P<0.05)。结论IFN-γ通过影响巨噬细胞活化水平,介导沙眼衣原体生殖道感染后的免疫应答,促进IL-1β、IL-17A分泌量﹐达到沙眼衣原体清除的目的。OBJECTIVE To explore the mechanism of interferon gamma(IFN-γ)in the mice with reproductive tract Chlamydia trachomatis infection.METHODS The reproductive tract infection models were obtained by vaginal in-oculation of mice with Chlamydia murine,the survival status of wild-type mice and IFN-γgene-deficient mice wasobserved,the body temperature,body weight,blood cell classification and counting and Cm inclusion bodiescounts were measured,the pathological damage of reproductive tract tissue was observed,and the levels of peripheral blood T lymphocyte subsets(CD3^(+),CD4^(+),CD8^(+),CD4^(+)/CD8^(+)),immunoglobulins(IgG,IgM,IgA)andinterleukin(IL-1β,IL-17A,IL-12)were analyzed.RESULTS Two weeks after the mice were infected with Cm,their survival status was poor.The body temperature of the mice was significantly higher in the non-interferencegene defect group than in the wild group and the gene defect group injected with IFN-γ(P<0.05);the bodyweight was significantly lower in the non-interference gene defect group than in the wild group and the gene defectgroup injected with IFN-γ(P<0.05);the macrophage level was significantly lower in the non-interference genedefect group than in the wild group and the gene defect group injected with IFN-γ(P<0.01).The Cm inclusionbody counts of the non-interference gene defect group were the highest,followed by the wild group,the gene defect group injected with IFN-γthe lowest(P<0.01).The levels of peripheral blood IL-17A,IgG and IgM of thenon-interference gene defect group were the lowest,and the levels of immune factors of the gene-deficient groupinjected with IFN-γwere similar to those of the wild group(P<0.05).CONCLUSION IFN-γmediates the immune response by affecting the activation level of macrophages after the genital tract infection of C.trachomatisand promotes the secretion of IL-1βand IL-17A so as to eliminate the C.trachomatis.

关 键 词:Γ干扰素 沙眼衣原体 生殖道感染 

分 类 号:R374[医药卫生—病原生物学]

 

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