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Immune cells sense and transduce mechanical signals such as stiffness, stretch, compression, and shear stress. In the past few years, our understanding of the mechanosensitive signaling pathways in myeloid cells has significantly expanded, especially in monocytes, macrophages, and dendritic cells. Recently, the mechanobiological regulation of neutrophil function has been deciphered. Mechanical signals from tissue-derived shear stress and cellular deformation tension reprogram neutrophil transcription via GEF-H1, PIEZO1, and TRPV4 pathways, modulating neutrophil functions in homeostasis and trans-endothelial migration. Understanding these force-dependent processes provides novel insights into neutrophil plasticity and highlights potential therapeutic strategies and approaches for inflammatory and infectious diseases.
Zhao et al. (Sun,) studied this question.