Arvand M, Ignatius R, Regnath T, Hahn H, Mielke M E
Department of Medical Microbiology, Institute of Infectious Diseases, Free University of Berlin, Berlin, Germany.
Infect Immun. 2001 Oct;69(10):6427-33. doi: 10.1128/IAI.69.10.6427-6433.2001.
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.
在使用C57BL/6小鼠的鼠感染模型中，研究了免疫活性宿主对汉赛巴尔通体感染的免疫反应。用人源汉赛巴尔通体菌株柏林-1进行腹腔感染后，在感染后的第一周内可从肝脏和脾脏中回收活菌，而感染后长达12周肝脏中通过PCR仍可检测到巴尔通体DNA。感染小鼠的肝脏中出现肉芽肿性病变，在感染后12周达到最大密度，并持续长达20周，表明汉赛巴尔通体在免疫活性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试验以及免疫球蛋白G（IgG）同种型分析，在体外分析了T细胞介导的免疫反应。感染小鼠的脾细胞在用热灭活的巴尔通体抗原刺激后特异性增殖。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周达到峰值，此后下降。感染动物的脾细胞在用巴尔通体抗原刺激后在体外产生γ干扰素，但不产生白细胞介素-4。感染小鼠血清中在2周时可检测到巴尔通体特异性IgG，抗体浓度在感染后12周达到峰值。IgG2b是巴尔通体特异性血清IgG抗体中的主要同种型。这些数据表明，汉赛巴尔通体在免疫活性C57BL/6小鼠中诱导具有Th1表型的细胞介导免疫反应。
