Solis, Angel G. and Bielecki, Piotr and Steach, Holly R. and Sharma, Lokesh and Harman, Christian C. D. and Yun, Sanguk and de Zoete, Marcel R. and Warnock, James N. and To, S. D. Filip and York, Autumn G. and Mack, Matthias and Schwartz, Martin A. and Dela Cruz, Charles. S. and Palm, Noah W. and Jackson, Ruaidhri and Flavell, Richard A. (2019) Mechanosensation of cyclical force by PIEZO1 is essential for innate immunity. NATURE, 573 (7772). 69-+. ISSN 0028-0836, 1476-4687
Full text not available from this repository. (Request a copy)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.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | ENDOTHELIN-1 GENE; HYPOXIA; EXPRESSION; SIGNAL; MECHANOTRANSDUCTION; MACROPHAGES; MECHANISMS; RECEPTORS; SUCCINATE; FIBROSIS; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Abteilung für Nephrologie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 06 Apr 2020 09:36 |
| Last Modified: | 06 Apr 2020 09:36 |
| URI: | https://pred.uni-regensburg.de/id/eprint/26274 |
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