Mechanosensation of cyclical force by PIEZO1 is essential for innate immunity

Angel G. Solis, Piotr Bielecki, Holly R. Steach, Lokesh Sharma, Christian C. D. Harman, Sanguk Yun, Marcel R. Zoete, James N. Warnock, S. D. Filip To, Autumn G. York, Matthias Mack, Martin A. Schwartz, Charles. S. Cruz, Noah W. Palm, Ruaidhrí Jackson () and Richard A. Flavell ()
Additional contact information
Angel G. Solis: Yale University School of Medicine
Piotr Bielecki: Yale University School of Medicine
Holly R. Steach: Yale University School of Medicine
Lokesh Sharma: Pulmonary, Critical Care and Sleep Medicine, Yale School of Medicine
Christian C. D. Harman: Yale University School of Medicine
Sanguk Yun: Yale University
Marcel R. Zoete: Utrecht University
James N. Warnock: University of Georgia
S. D. Filip To: Mississippi State University
Autumn G. York: Yale University School of Medicine
Matthias Mack: University Hospital Regensburg
Martin A. Schwartz: Yale University
Charles. S. Cruz: Pulmonary, Critical Care and Sleep Medicine, Yale School of Medicine
Noah W. Palm: Yale University School of Medicine
Ruaidhrí Jackson: Yale University School of Medicine
Richard A. Flavell: Yale University School of Medicine

Nature, 2019, vol. 573, issue 7772, 69-74

Abstract: 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.

Date: 2019
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DOI: 10.1038/s41586-019-1485-8

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