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TRPV1+神经元促进皮肤免疫力,对抗Schistosoma mansoni的疾病

Juan M Inclan-Rico, Adriana Stephenson, Camila M Napuri

bioRxiv : the preprint server for biology

|February 20, 2025

概括

寄生虫虫Schistosoma mansoni抑制了皮肤中疼痛感应神经的激活. 这种免疫规避使寄生虫能够传播并引起慢性感染.

科学领域:

免疫学免疫学免疫学
神经科学是一个神经科学.
寄生虫学的寄生虫学

背景情况:

皮肤免疫力依赖于检测病原体.
寄生虫虫 Schistosoma mansoni 经常在皮肤中逃避最初的免疫检测.
疼痛感应神经元表达短暂受体潜在化物1 (TRPV1) 是检测皮肤入侵者的关键.

研究的目的:

为了研究TRPV1+神经元在宿主对Schistosoma mansoni的免疫反应中的作用.
了解Schistosoma mansoni如何与TRPV1+介导免疫相互作用并潜在地逃避免疫.

主要方法:

使用了Schistosoma mansoni感染的小鼠模型.
采用了功能增加和丧失的遗传方法来研究TRPV1+神经元活动.
测量了对刺激的行为反应,流入和神经释放在感觉神经元中.
评估免疫细胞群 (γδ T 细胞,中性粒细胞,单细胞) 和皮肤中细胞因子的产生.

主要成果:

被 Schistosoma mansoni 感染的小鼠对疼痛刺激的反应有所减少.
感染小鼠的感觉神经元在素刺激后表现出减少的流和神经释放.
TRPV1+神经元对于控制Schistosoma mansoni在从皮肤迁移期间的生存至关重要.
TRPV1+神经元促进了免疫细胞在皮肤中的积累和激活,包括γδ T细胞,中性粒细胞和单细胞.

结论:

曼索尼杆菌 (Schistosoma mansoni) 积极抑制TRPV1+神经元的激活,作为逃避免疫检测的机制.
这种抑制限制了IL-17介导的炎症,促进了寄生虫的传播和慢性感染.
TRPV1+神经元在启动对Schistosoma mansoni的保护性皮肤免疫力方面发挥着至关重要的作用.

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