首页> 外文期刊>The Journal of Infectious Diseases >Suppression of acute Ixodes scapularis-induced Borrelia burgdorferi infection using tumor necrosis factor-alpha, interleukin-2, and interferon-gamma.
【24h】

Suppression of acute Ixodes scapularis-induced Borrelia burgdorferi infection using tumor necrosis factor-alpha, interleukin-2, and interferon-gamma.

机译:使用肿瘤坏死因子-α,白细胞介素-2和干扰素-γ抑制肩I小舌虫引起的伯氏疏螺旋体感染。

获取原文
获取原文并翻译 | 示例
           

摘要

Down-regulation of mammalian cytokine production has been demonstrated during tick feeding. To examine the hypothesis that reconstitution of cytokines during tick feeding could facilitate immune containment of Borrelia burgdorferi, the following experiments were done. C3H/HeJ mice were given cytokines for 10 days after Ixodes scapularis attachment. At day 21, ear biopsies were analyzed for B. burgdorferi. Polymerase chain reaction analysis indicated a protection rate of 95% in mice receiving tumor necrosis factor (TNF)-alpha. Mice that received interleukin (IL)-2 or interferon (IFN)-gamma had infection rates of 30%-45% compared with 83% for untreated controls. No correlation was noted between neutralizing antibody, reactivity by Western blot, and subsequent protection. Culture of B. burgdorferi in cytokine-conditioned media indicated that TNF-alpha, IFN-gamma, and IL-2 were not cytotoxic for B. burgdorferi. These data suggest that cytokine-induced protection from B. burgdorferi infection was immune-mediated and that cellular immunity may be associated with protection from I. scapularis-induced infection.
机译:tick喂养期间已证明哺乳动物细胞因子产生的下调。为了检验关于tick喂养期间细胞因子重构可以促进伯氏疏螺旋体免疫抑制的假说,进行了以下实验。肩x突棘附着后,将C3H / HeJ小鼠的细胞因子给予10天。在第21天,分析耳活组织检查中的伯氏疏螺旋体。聚合酶链反应分析表明,接受肿瘤坏死因子(TNF)-α的小鼠的保护率达到95%。接受白介素(IL)-2或干扰素(IFN)-γ的小鼠感染率为30%-45%,而未经治疗的对照组为83%。在中和抗体,通过蛋白质印迹的反应性和随后的保护之间未发现相关性。在细胞因子条件培养基中对B. burgdorferi进行培养表明,TNF-α,IFN-γ和IL-2对B. burgdorferi没有细胞毒性。这些数据表明,细胞因子诱导的对伯氏疏螺旋体感染的保护是免疫介导的,并且细胞免疫可能与对肩骨诱导的感染的保护相关。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号