BackgroundNeutrophils play an important role in the immune system by sensing environmental perturbations, including pathogens. Upon activation, neutrophils extrude their chromatin to form neutrophil extracellular traps (NETs), which trap and remove pathogens.
Chromatin decondensation during NET formation is a regulated process that reflects both the inducing pathways and the cellular environment. However, most studies rely on non-physiological stimuli like phorbol 12-myristate 13-acetate (PMA), which bypass key regulatory mechanisms.
As a result, how physiologically relevant inflammatory signals change neutrophil chromatin accessibility and relate to disease associated transcriptional states remains poorly understood.MethodsWe used the Assay for Transposase-Accessible Chromatin with sequencing (ATAC-Seq) to profile chromatin accessibility in neutrophils stimulated in whole blood with PMA and physiologically relevant inflammatory natural factors (NFs), including TNF-α, GM-CSF, fMLP, C5a, and IL-1β, alone and in combination. Chromatin responses were compared across conditions and integrated with publicly available transcriptomic sepsis cohorts.ResultsNF stimulation induced stimulus specific chromatin accessibility programs distinct from PMA.
Frontiers in Immunology published a clinical update in Infectious Disease on 10 Jun 2026.
The item focuses on Cytokine-induced chromatin accessibility in whole blood neutrophils links to sepsis transcriptional states.
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