通过病原体抑制厌食症促进宿主生存和传播
Sheila Rao1, Alexandria M Palaferri Schieber1, Carolyn P O'Connor2
1Nomis Center for Immunobiology and Microbial Pathogenesis, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Cell
|January 28, 2017
概括
沙门氏菌感染通过操纵肠脑轴来预防疾病引起的厌食症. 这种抑制通过降低毒性来提高宿主生存率和病原体传播.
科学领域:
- 微生物学
- 免疫学
- 神经科学
背景情况:
- 疾病引起的厌食症是宿主对感染的常见反应.
- 肠-大脑轴在疾病行为中起着至关重要的作用.
研究的目的:
- 调查沙门氏菌如何操纵肠-大脑轴以抑制疾病诱发的厌食症.
- 了解S. Typhimurium效应物SlrP在这个过程中的作用.
主要方法:
- 在宿主中使用沙门氏菌 Typhimurium 感染模型.
- 研究了SlrP效应器和炎症酶激活的作用.
- 检查了涉及IL-1β,下丘脑和迷走神经的信号通路.
主要成果:
- S. Typhimurium SlrP 抑制了炎症酶的激活,防止了因IL-1β信号传递而引起的厌食症.
- 受病原体诱导的厌食症抑制提高了宿主存活率和减少了全身感染.
- 这种抑制也增加了病原体向新宿主的传播.
结论:
- 微生物可以进化机制来调节疾病行为,有利于宿主健康和病原体传播.
- 病原体毒性和传播之间存在权衡,受宿主行为调节的影响.
- 抑制厌食症是S. Typhimurium的毒性策略,它促进了自身的繁殖.
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