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来自Vibrio vEP-45蛋白酶的C-ter100作为一种与病原体相关的分子模式,诱导炎症和天生的免疫力

Jung Eun Park^1,2, Ji-Hye Yun^3,4, Weontae Lee³

¹Department of Biomedical Science, College of Natural Sciences and Public Health and Safety, Chosun University, Gwangju, Republic of Korea.

|August 26, 2024

概括

来自Vibrio vulnificus的C-ter100激活了通过结合TLR4和NLRP3来激活天生的免疫力,导致炎症. 这种与病原体相关的分子模式可以作为新抗生素开发的目标.

科学领域:

微生物学微生物学
免疫学免疫学免疫学
生物化学生物化学

背景情况:

性会导致人类致命的败血症.
vEP-45蛋白酶的自我蛋白解产生了vEP-34和C-ter100.
vEP-45和vEP-34激活了血液凝固和卡利克林/基宁系统.

研究的目的:

研究C-ter100在炎症和宿主天生的免疫激活中的作用.
确定C-ter100诱导炎症反应的分子机制.

主要方法:

在体外测试评估NF-κB激活,TLR4结合和炎症酶激活 (NLRP3,ASC,caspase1).
测量细胞因子 (TNF-α) 和氧化 (NO) 分泌.
在小鼠体内研究以评估免疫细胞的招募和基因组胺的释放.
使用抗C-ter100单克隆抗体 (C-ter100Mab) 的中和试验.

主要成果:

C-ter100通过TLR4激活NF-κB,促进TNF-α和NO分泌.
C-ter100 激活NLRP3炎症酶,导致IL-1β分泌.
在小鼠中,C-ter100诱导了中性粒细胞和单细胞的招募和胰岛素的释放.
一种抗C-ter100单克隆抗体有效中和C-ter100诱导的炎症.

结论:

C-ter100作为一种与病原体相关的分子模式 (PAMP) 起作用,在病毒感染期间触发天生的免疫反应.
C-ter100是V. vulnificus引起的炎症的关键调解者.
C-ter100代表了一个潜在的治疗点,用于开发新型抗生素来对抗Vibrio感染.

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