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由Litomosoides sigmodontis microfilariae诱导的埃索诺菲尔ETosis依赖于正规的炎症细胞路径

Alexandra Ehrens¹, Benjamin Lenz², Celia Nieto-Pérez²

¹Institute for Medical Microbiology, Immunology and Parasitology, University Hospital Bonn, 53127 Bonn, Germany; German Center for Infection Research (DZIF), Partner Site Bonn-Cologne, Bonn, Germany.

|January 8, 2025

概括

微纤维菌 (MF) 通过规范性炎症体路径触发了细胞防御机制 - - 乙氨基基细胞ETosis. 这一途径涉及关键的炎细胞组分,对于对寄生虫虫的反应中DNA释放至关重要.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
寄生虫学的寄生虫学

背景情况:

颗粒细胞利用效应机制,如ETosis (细胞外陷形成).
细菌性ETosis涉及非正规的炎症体路径.
炎症体在对细胞外病原体的ETosis中的作用仍然不清楚.

研究的目的:

为了研究微菌 (MF) 诱导的氨基酸ETosis中的炎症体路径.
为了确定在这个过程中涉及的特定的炎症组分.

主要方法:

用于研究MF诱导的ETosis,采用了小鼠乙氨基酸.
他们使用了炎症组分 (gasdermin D,caspase-1,ASC,AIM2) 的遗传淘汰.
评估了DNA释放,反应性氧物种生成和核膜崩.

主要成果:

微纤维菌 (MF) 通过正规的炎症酶路径诱导欧诺菲尔ETosis.
缺少气体皮质D,酶-1,ASC或AIM2可以防止MF诱导的DNA释放.
在ETosis的后期阶段,AIM2对于DNA释放至关重要,但对于ROS生成或核膜崩至关重要.
这些发现在人类的乙氨基细胞中得到证实.

结论:

规范性炎症体通路对于微细菌菌诱导的埃索诺菲尔体中ETosis至关重要.
在ETosis过程中,AIM2在DNA挤出中发挥着特定的作用.
这种机制在小鼠和人类氨酸细胞之间保持着.

关键词:

在AIM2中,AIM2是AIM2.CP: 免疫学免疫学 CP: 微生物学微生物学 ETosis ETosis 是一种与生俱来的过程.GSDMDMD的总体发展目标是什么卡斯帕斯-1酶是一种埃索诺菲尔细胞的存在类动物 (filariae) 是一种类动物.一些炎症一些炎症

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