中国媒介生物学及控制杂志 ›› 2012, Vol. 23 ›› Issue (2): 128-131.

• 论著 • 上一篇    下一篇

组氨酸激酶Ⅱ在伯氏疏螺旋体生活史中的功能

杨章女1, 蒋宝贵2, 杨晓峰3, 徐海君4, 曹务春2   

  1. 1. 浙江省疾病预防控制中心出血热重点实验室, 杭州310051;
    2. 军事医学科学院微生物流行病研究所;
    3. 印第安纳大学医学院;
    4. 浙江大学昆虫科学研究所, 杭州310058
  • 收稿日期:2011-11-04 出版日期:2012-04-20 发布日期:2012-04-20
  • 通讯作者: 徐海君,Email: haijunxu@zju.edu.cn
  • 作者简介:杨章女(1980-),女,主管技师,主要从事微生物生化研究。Email: yangzhangnv@163.com
  • 基金资助:

    中央高校基本科研业务费专项资金资助(3A6000*172210111)

The function of histidine kinaseⅡ(Hk2) in the life cycle of Borrelia burgdorferi

YANG Zhang-nv1, JIANG Bao-gui2, YANG Xiao-feng3, XU Hai-jun4, CAO Wu-chun2   

  1. 1. Zhejiang Center for Disease Control and Prevention, Hangzhou 310051, Zhejiang Province, China;
    2. Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences;
    3. Indiana University School of Medicine;
    4. Institute of Insect Science, Zhejiang University, Hangzhou 310058, Zhejiang Province, China
  • Received:2011-11-04 Online:2012-04-20 Published:2012-04-20
  • Supported by:

    Supported by the Fundamental Research Funds for the Central Universities(No. 3A6000*172210111)

摘要:

目的 伯氏疏螺旋体组氨酸激酶Ⅱ(Hk2)和反应调节蛋白Rrp2共同组成一个二元信号系统,控制病原菌侵染哺乳动物所需致病因子的表达,但Hk2的生物学功能有待验证。方法 应用同源重组方法得到hk2 敲除菌株(hk2-),并利用蜱-鼠动物模型对其生物学功能进行探索。结果 hk2-能够通过人工针刺正常感染小鼠,间接免疫荧光试验显示在吸血的幼蜱和若蜱中肠能够检测到hk2-,定量PCR结果显示hk2 敲除并不影响病原菌在若蜱中肠的繁殖,但在蜱叮咬状态下只有50%的小鼠能够被hk2-感染。结论 Hk2不影响病原菌从鼠传播到幼蜱及随后在蜱体内的长期寄生,但hk2 敲除降低了病原菌在自然条件下(蜱叮咬)感染小鼠的能力,研究结果暗示Hk2在病原菌生活史中的功能是协助病原菌高效地侵染哺乳动物。

关键词: 伯氏疏螺旋体, 组氨酸激酶Ⅱ, 动物模型

Abstract:

Objective To validate the biological function of Hk2,which is reported to be in combination with the cognate response regulator Rrp2 to constitute a two component signal system in Borrelia burgdorferi that controls the key virulence factors required for pathogen invasion in mammals. Methods A hk2 knockout strain (hk2-) was generated through homologous recombination, with the biological function of Hk2 estimated by the mouse-tick animal model. Results The hk2- knockout strain remained to be able to infect mouse by needle inoculation, and subsequently successfully detected in the midgut of fed-larvae and -nymph by IFA. The quantitative-PCR demonstrated that hk2 knockout had no influence on bacterial replication in the midgut of fed nymph. However, only 50% of tested mice were infected in hk2- group by tick bite. Conclusion The hk2 knockout does not affect the pathogen acquisition from mouse by larvae ticks and subsequent persistent colonization in tick midgut, but it embarrasses the transmission from nymph to mouse under natural conditions by tick bite. The above data indicate that the Hk2 may effectively contribute to the pathogen invading mammals in the life cycle of B. burgdorferi.

Key words: Borrelia burgdorferi, Histidine kinaseⅡ, Animal model

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