在细胞极性变化的Helicobacter pylori和爱斯坦-巴尔病毒感染
Budhadev Baral1, Meenakshi Kandpal1, Anushka Ray1
1Infection Bioengineering Group, Department of Biosciences and Biomedical Engineering, Indian Institute of Technology Indore, Simrol, Indore, Madhya Pradesh, 453552, India.
Folia microbiologica
|September 6, 2023
概括
细胞极性蛋白维持细胞不对称性,这对于防御诸如Helicobacter pylori和爱斯坦-巴尔病毒等病原体至关重要. 失去极性会促进感染和癌症的进展,特别是在共感染中.
科学领域:
- 细胞生物学 细胞生物学
- 微生物学 微生物学
- 在瘤学瘤学.
背景情况:
- 细胞极性,由特定的蛋白质组维持,对于宿主防御病原体至关重要.
- 细胞极性丧失与增加感染易感性和癌症进展有关.
- 杆菌 (H. pylori) 和爱斯坦-巴尔病毒 (EBV) 是致癌物,可以改变宿主细胞的极性.
研究的目的:
- 审查H. pylori和EBV在上皮细胞中破坏细胞极性的机制.
- 讨论H. pylori和EBV如何针对宿主细胞的极性复合体来产生病原体.
- 探索放松调节的分子通路在联合感染引起的胃癌中的作用.
主要方法:
- 关于细胞极性,H. pylori和EBV感染的研究的文献综述.
- 对H. pylori和EBV蛋白质影响细胞极性性的分子机制的分析.
- 检查参与极性复杂调制的信号通路 (NF-κB,TGF-β/SMAD,β-catenin).检查极性复杂调制中的信号通路.
主要成果:
- 杆菌蛋白质 (CagA,VacA,OipA,尿酶) 和EBV基因 (LMP1,LMP2A,LMP2B,EBNA3C,EBNA1) 破坏细胞平衡和极性.
- 与H. pylori和EBV的同时感染会导致一种更具侵略性的胃癌.
- 这些病原体准并调节关键极性复合体,如PAR,SCRIB和CRB.
结论:
- 杆菌和EBV通过各种蛋白质和基因在感染的上皮细胞中积极变形细胞极性.
- 细胞极性失调是H. pylori和EBV病原和相关癌症的关键因素.
- 了解这些机制为治疗由这些病原体驱动的感染和癌症提供了洞察力.
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