...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >Mechanism of pertussis toxin B oligomer-mediated protection against Bordetella pertussis respiratory infection.
【24h】

Mechanism of pertussis toxin B oligomer-mediated protection against Bordetella pertussis respiratory infection.

机译：百日咳毒素B寡聚物介导的针对百日咳博德特氏菌呼吸道感染的保护机制。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Immunization with the B oligomer of pertussis toxin protected neonatal mice from a lethal respiratory challenge with Bordetella pertussis. All mice immunized with 8 micrograms of B oligomer survived aerosol challenge and had peripheral leukocyte counts and weight gains similar to those of mice immunized with pertussis toxoid before challenge and to those of control mice that were not challenged. Unprotected mice challenged with an aerosol of B. pertussis had an increase in peripheral leukocyte count, failed to gain weight, and died within 21 days of challenge. Protection appeared to be dose dependent, since a dose of 1 microgram of B oligomer per mouse prevented death in 100% of the mice challenged with B. pertussis, whereas 0.4 micrograms of B oligomer protected 50% of the challenged mice. Mice immunized with the B oligomer had increases in immunoglobulin G (IgG) anti-B oligomer in sera and in IgG and IgA anti-B oligomer in bronchoalveolar lavage fluids 1 to 3 weeks after respiratory challenge. Specific anti-B oligomer antibodies could not be detected in unimmunized, infected mice at the same time after challenge. Intravenous administration of the monoclonal antibody 170C4, which binds to the S3 subunit of the B oligomer, protected neonatal mice from B. pertussis respiratory challenge, while administration of an IgG1 anti-tetanus toxin monoclonal antibody, 18.1.7, was not protective. We conclude that anti-B-oligomer-mediated neutralization of pertussis toxin is one mechanism of protection in the mouse model of B. pertussis aerosol challenge.
机译：百日咳毒素B低聚物的免疫保护了新生小鼠免受百日咳博德特氏菌的致死性呼吸道攻击。用8微克B寡聚体免疫的所有小鼠均在气溶胶攻击中幸存下来，并且外周血白细胞计数和体重增加与攻击前用百日咳类毒素免疫的小鼠和未攻击的对照小鼠相似。用百日咳博德特氏菌气雾剂攻击的未保护小鼠外周血白细胞计数增加，体重增加失败，并在攻击后21天内死亡。保护似乎是剂量依赖性的，因为每只小鼠1微克B寡聚体的剂量可防止百日咳博德特氏菌攻击的小鼠死亡，而0.4微克B寡聚体可保护50％的受攻击小鼠死亡。呼吸激发后1至3周，用B低聚物免疫的小鼠血清中的免疫球蛋白G（IgG）抗B低聚物以及支气管肺泡灌洗液中的IgG和IgA抗B低聚物增加。在攻击后的同一时间，在未免疫的感染小鼠中未检测到特异性抗B寡聚体抗体。静脉内施用与B寡聚体的S3亚基结合的单克隆抗体170C4，可以保护新生小鼠免受百日咳博德特氏菌呼吸道攻击，而IgG1抗破伤风毒素单克隆抗体18.1.7则无保护作用。我们得出的结论是，抗B-寡聚体介导的百日咳毒素中和是百日咳博德特氏菌气溶胶激发小鼠模型中的一种保护机制。

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