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展开的蛋白质反应是Campylobacter jejuni病原和宿主防御的关键调解者

Geunhye Hong¹, Zahra Omole¹, Cadi Davies¹

¹Faculty of Infectious and Tropical Diseases, London School of Hygiene & Tropical Medicine, Keppel Street, London, United Kingdom.

Microbes and infection

|October 30, 2025

概括

坎比洛巴克特 (Campylobacter jejuni) 感染激活了人类肠道细胞中的未折叠蛋白质反应 (UPR). 这种由C. jejuni的UPR激活,受其囊和鞭毛的影响,影响炎症和病原体的生存.

科学领域:

微生物学微生物学
细胞生物学细胞生物学
免疫学免疫学免疫学

背景情况:

全球范围内,Campylobacter jejuni是导致细菌性食物传播疾病的首要原因.
C. jejuni与人类肠上皮细胞 (IECs) 之间的相互作用,特别是宿主防御机制,如未折叠的蛋白质反应 (UPR),尚未完全理解.
UPR是一种细胞应激反应,该应激反应是对内质网膜中错误折叠的蛋白质的反应,已知受病原体操纵.

研究的目的:

调查UPR是否是C. jejuni在入侵人类IEC时利用的毒性机制.
确定UPR激活在C. jejuni病原和宿主炎症反应中的作用.

主要方法:

在C. jejuni感染后的IEC中评估了UPR激活标志物 (PERK,IRE1α,ATF6).
利用化学诱导剂和UPR抑制剂研究其对C. jejuni细胞内生存和IL-8释放的影响.
研究了C. jejuni囊多糖和鞭毛对使用细菌突变物激活UPR的贡献.

主要成果:

在C. jejuni感染中,PERK和IRE1α的调节一直在上升,ATF6的激活因菌株和细胞系而异.
化学诱导UPR降低了细胞内C. jejuni的存活率,而抑制UPR则增加了存活率并减少了IL-8的释放.
缺乏囊多糖或鞭毛的C. jejuni突变体在IECs中显示了减少的UPR激活.

结论:

UPR激活是C. jejuni感染期间的主体反应,受囊和鞭毛等细菌因素的影响.
C. jejuni似乎利用或调节UPR,影响细菌生存和宿主炎症 (IL-8释放).
这些发现提供了关于C. jejuni病变发生,UPR调节和感染期间宿主炎症反应的见解.

关键词:

坎比洛巴克特 (Campylobacter jejuniuni) 是一个常见的细菌.压力ERER压力ERER压力炎症炎症是一种炎症.不折叠的蛋白质反应反应

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