细菌激活感官神经元,调节疼痛和炎症
Isaac M Chiu1, Balthasar A Heesters, Nader Ghasemlou
1Kirby Neurobiology Center, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Nature
|August 23, 2013
概括
细菌直接激活疼痛感应神经元,在感染期间引起疼痛. 这种疼痛感觉独立于免疫反应,揭示了神经系统在宿主-病原体相互作用中的直接作用.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
背景情况:
- nociceptor神经元检测有害的刺激,启动疼痛和防御行为.
- 细菌感染通过不太了解的机制引起疼痛,通常被认为是免疫介导的.
研究的目的:
- 研究细菌激活 nociceptors并诱导疼痛的直接机制.
- 确定免疫系统在细菌感染引起的疼痛中的作用.
主要方法:
- 使用老鼠模型感染金黄色葡萄球菌.
- 评估了机械和热性过敏症.
- 通过成像和电生理学研究神经元激活.
- 研究了特定细菌成分 (N-formylated,α-haemolysin) 的作用.
- 使用了Nav1.8系神经元的遗传切除.
主要成果:
- 在小鼠中,细菌感染引起的疼痛与TLR2,MyD88,T细胞,B细胞,中性粒细胞和单细胞无关.
- 与活细菌负载相关的疼痛和过敏症,而不是胀或免疫标志物.
- 细菌通过N-formylated和α-haemolysin直接诱导的流量和作用潜力在恶性受体中.
- 切除Nav1.8神经元可以减少疼痛,但会增加局部免疫透和淋巴腺病变.
结论:
- 细菌直接激活 nociceptors,在感染期间启动疼痛.
- 感官神经元在宿主-病原体相互作用期间调节炎症方面发挥着意想不到的作用.
- 病原体激活神经系统是宿主反应的关键组成部分.
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