坎皮洛巴克特 (Campylobacter jejuni) 调节细胞循环的进展,以增强宿主细胞入侵的潜力
Prabhat K Talukdar1, Megan C Dines1, Eric A Shelden1
1School of Molecular Biosciences, College of Veterinary Sciences, Washington State University, Pullman, WA, 99164, USA.
Cell communication and signaling : CCS
|July 16, 2025
概括
坎比洛巴克特 (Campylobacter jejuni) 感染减缓了宿主细胞周期的进展,细菌优先侵入G1阶段细胞. 这种干扰会影响细胞因子的产生和肠道屏障的功能.
科学领域:
- 微生物学和免疫学
- 细胞生物学 细胞生物学
背景情况:
- 坎比洛巴克特 (Campylobacter jejuni) 通过入侵肠道细胞并触发宿主炎症反应,导致肠炎.
- 细菌入侵依赖于宿主细胞的焦点粘附元件,将细胞外基质连接到actin细胞骨架.
- 在C. jejuni的入侵中,它似乎与宿主细胞循环调节元件进行了接触.
研究的目的:
- 为了研究C. jejuni调节宿主细胞周期的假设.
- 了解C. jejuni入侵和宿主细胞周期阶段之间的关系.
- 确定C. jejuni感染对宿主基因表达和细胞因子产生的影响.
主要方法:
- 流细胞计分析细胞周期阶段 (G1,S,G2,M).
- 单细胞RNA测序 (scRNA-seq) 和RT-qPCR用于差异基因表达分析.
- 感染测定,共聚焦显微镜和ELISA测试以评估细菌入侵,局部化和IL-8分泌.
主要成果:
- 结核菌感染减缓了细胞周期的进展,并增加了G1阶段细胞的百分比.
- 宿主基因表达分析揭示了参与细胞循环调节的基因的上调,焦点粘附,炎症和氧化应激.
- C. jejuni优先入侵G1阶段细胞,在G1细胞中表现出增加的与帕克西林的同位化,并从感染的G1细胞中增加IL-8分泌.
结论:
- 坎皮洛巴克特 (Campylobacter jejuni) 改变了肠球细胞周期的进展,有利于在G1阶段的入侵.
- 感染导致细胞因子产生变化,并可能影响免疫细胞招募.
- 这些变化破坏了肠道的透性屏障,导致了急性野营菌病.
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