小柯机器人

机械压力可激活先天免疫
2019-08-22 12:59

美国耶鲁大学Richard A. Flavell和Ruaidhrí Jackson研究组合作发现PIEZO1介导的机械力感知在先天免疫中的作用。该项研究成果于2019年8月22日在线发表在《自然》上。

研究人员发现周期性静水压力(类似于免疫细胞在肺里的经历),通过机械性激活的离子通道PIEZO1引发炎症反应。在先天免疫细胞中缺乏PIEZO1的小鼠在细菌感染或纤维化自身炎症的情况下表现出降低的肺部炎症。这些研究结果揭示了一种环境感知信号轴,其能够刺激先天免疫细胞产生炎症反应,并证明了PIEZO1和机械力感知在免疫中的生理作用。

据悉,先天免疫细胞直接识别入侵病原体是炎症反应的关键驱动因素。然而,先天免疫系统的细胞也可以感知它们的局部微环境并响应温度、pH、氧气和营养物质可用性的生理波动,而这些波动在炎症期间会被改变。虽然免疫系统细胞在其整个生命周期中都经历了力和压力,但对这些机械过程如何调节免疫反应知之甚少。

附:英文原文

Title: Mechanosensation of cyclical force by PIEZO1 is essential for innate immunity

Author: Angel G. Solis, Piotr Bielecki, Holly R. Steach, Lokesh Sharma, Christian C. D. Harman, Sanguk Yun, Marcel R. de Zoete, James N. Warnock, S. D. Filip To, Autumn G. York, Matthias Mack, Martin A. Schwartz, Charles. S. Dela Cruz, Noah W. Palm, Ruaidhr Jackson, Richard A. Flavell

Issue&Volume: 2019-08-21

Abstract: Direct recognition of invading pathogens by innate immune cells is a critical driver of the inflammatory response. However, cells of the innate immune system can also sense their local microenvironment and respond to physiological fluctuations in temperature, pH, oxygen and nutrient availability, which are altered during inflammation. Although cells of the immune system experience force and pressure throughout their life cycle, little is known about how these mechanical processes regulate the immune response. Here we show that cyclical hydrostatic pressure, similar to that experienced by immune cells in the lung, initiates an inflammatory response via the mechanically activated ion channel PIEZO1. Mice lacking PIEZO1 in innate immune cells showed ablated pulmonary inflammation in the context of bacterial infection or fibrotic autoinflammation. Our results reveal an environmental sensory axis that stimulates innate immune cells to mount an inflammatory response, and demonstrate a physiological role for PIEZO1 and mechanosensation in immunity.

DOI: 10.1038/s41586-019-1485-8

Source:https://www.nature.com/articles/s41586-019-1485-8

Nature:《自然》,创刊于1869年。隶属于施普林格·自然出版集团,最新IF:69.504
官方网址:http://www.nature.com/
投稿链接:http://www.nature.com/authors/submit_manuscript.html


本期文章:《自然》:Online/在线发表

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