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首页> 美国卫生研究院文献>Infection and Immunity >Bartonella henselae-Specific Cell-Mediated Immune Responses Display a Predominantly Th1 Phenotype in Experimentally Infected C57BL/6 Mice
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Bartonella henselae-Specific Cell-Mediated Immune Responses Display a Predominantly Th1 Phenotype in Experimentally Infected C57BL/6 Mice

机译：汉赛巴尔通体特异性细胞介导的免疫反应在实验感染的C57BL / 6小鼠中显示主要是Th1表型。

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摘要

Immune responses of the immunocompetent host to Bartonella henselae infection were investigated in the murine infection model using C57BL/6 mice. Following intraperitoneal infection with human-derived B. henselae strain Berlin-1, viable bacteria could be recovered from livers and spleens during the first week postinfection, while Bartonella DNA remained detectable by PCR in the liver for up to 12 weeks after infection. Granulomatous lesions developed in livers of infected mice, reached maximal density at 12 weeks after infection, and persisted for up to 20 weeks, indicating that B. henselae induced a chronic granulomatous hepatitis in the immunocompetent murine host. T-cell-mediated immune responses were analyzed in vitro by means of spleen cell proliferation and cytokine release assays as well as analysis of immunoglobulin G (IgG) isotypes. Spleen cells from infected mice proliferated specifically upon stimulation with heat-killed Bartonella antigen. Proliferative responses were mainly mediated by CD4+ T cells, increased during the course of infection, peaked at 8 weeks postinfection, and decreased thereafter. Gamma interferon, but not interleukin-4, was produced in vitro by spleen cells from infected animals upon stimulation with Bartonella antigens. Bartonella-specific IgG was detectable in serum of infected mice by 2 weeks, and the antibody concentration peaked at 12 weeks postinfection. IgG2b was the prominent isotype among the Bartonella-specific serum IgG antibodies. These data indicate that B. henselae induces cell-mediated immune responses with a Th1 phenotype in immunocompetent C57BL/6 mice.
机译：使用C57BL / 6小鼠在小鼠感染模型中研究了有免疫能力的宿主对汉氏巴尔通体感染的免疫反应。腹膜内感染人源性B. henselae菌株Berlin-1后，可在感染后的第一周从肝脏和脾脏中回收活菌，而感染后长达12周的肝脏中仍可通过PCR检测到巴尔通体DNA。肉芽肿性病变在受感染小鼠的肝脏中发展，在感染后12周达到最大密度，并持续长达20周，这表明亨氏芽孢杆菌在具有免疫能力的小鼠宿主中诱发了慢性肉芽肿性肝炎。通过脾细胞增殖和细胞因子释放测定以及免疫球蛋白G（IgG）同种型的分析，在体外分析T细胞介导的免疫反应。受热灭活的巴尔通体抗原刺激后，感染小鼠的脾细胞特异性增殖。增殖反应主要由CD4 + T细胞介导，在感染过程中增加，在感染后8周达到高峰，然后降低。巴尔通体抗原刺激后，来自感染动物的脾细胞在体外产生了γ-干扰素，但没有白介素-4。在感染小鼠的血清中检测到Bartonella特异性IgG的时间为2周，并且抗体浓度在感染后12周达到峰值。 IgG2b是Bartonella特异性血清IgG抗体中的主要同种型。这些数据表明，亨氏芽孢杆菌在具有免疫能力的C57BL / 6小鼠中诱导具有Th1表型的细胞介导的免疫反应。

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