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Neutrophils are a type of innate immune cell that contains distinctive cytoplasmic granules and a nucleus that is divided into three segments. They are the most abundant immune cell type in the blood. Neutrophils are rapidly recruited to infected tissues and can engulf bacteria directly or produce toxic antimicrobial mediators.
Neutrophils are involved in both the initiation and resolution of cardiac inflammation post myocardial infarction (MI). Here, the authors show that intravenously injected nanoparticles can modulate cardiac neutrophils to inhibit inflammation and promote repair for MI therapy.
Neutrophils undergo shear stress in the circulation and mechano-sensing is known to impact neutrophil biology. Here the authors show that activation of Piezo1 by shear stress triggers a sequence of cellular events leading to NETosis.
Neutrophil extracellular traps (NETs) play multifaceted roles in numerous neutrophil-mediated diseases. The authors show that inhibiting cathepsin C ameliorates ANCA-associated vasculitis, a NET-related disorder, by reducing neutrophil serine protease activity and NET formation in a rat model.
The mechanisms by which stroke and myocardial infarction trigger lymphocyte loss remain poorly defined. This study shows that the release of neutrophil extracellular traps (NETs) after stroke and myocardial infarction triggers B cell apoptosis and reduces the number of IgA-producing plasma cells. Therapeutic targeting of NETs is immunoprotective in mice and humans.
In this recent study, He et al. establish that chronic stress promotes metastasis through stress-induced formation of neutrophil extracellular traps (NETs).
