A recent study published in Nature Cell Biology reveals that chromatin decompaction within the nucleus of neutrophils increases plasma membrane tension, which promotes the execution of NETosisβa process where neutrophils release extracellular traps to fight pathogens. This mechanism operates independently of transcription.
The research, led by the Thiam lab at Stanford University, demonstrates that the physical state of chromatin, not just its genetic activity, influences cellular mechanics. By decompacting chromatin, the nucleus expands, which in turn stretches the plasma membrane, raising its tension. This tension is a critical signal that triggers the final steps of NETosis.
NETosis is a double-edged sword: it helps trap and kill microbes, but excessive NETosis is linked to autoimmune diseases and thrombosis. Understanding the mechanical triggers could lead to new therapeutic strategies for modulating NETosis in disease.
The findings were supported by discussions with experts including Christine Jacobs Wagner and Henry de Belly, and imaging was performed at the Stanford University Cell Sciences Imaging Facility. The study was published on August 19, 2026.
