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Mitochondria sense bacterial lactate and drive release of neutrophil extracellular traps.
Cell Host Microbe
February 2025
Department of Microbiology, University of Tennessee, Knoxville, TN, USA; Department of Biochemistry & Cellular and Molecular Biology, University of Tennessee, Knoxville, TN, USA. Electronic address:
Neutrophils induce oxidative stress, creating a harsh phagosomal environment. However, Staphylococcus aureus can survive these conditions, requiring neutrophils to deploy mechanisms that sense bacterial persistence. We find that staphylococcal lactate is a metabolic danger signal that triggers neutrophil extracellular trap release (NETosis).
View Article and Find Full Text PDFImplications of NETosis in Diabetic Wound Healing.
Curr Pharm Des
February 2025
Centre for Research Impact & Outcome-Chitkara College of Pharmacy, Chitkara University, Rajpura, Punjab 140401, India.
The Role of Crosstalk between Nets and Keratinocytes in Skin Immunity.
J Invest Dermatol
February 2025
Department of Dermatology, The Second Xiangya Hospital of Central South University, Hunan Key Laboratory of Medical Epigenomics, Changsha, China. Electronic address:
The skin is the principal barrier against pathogens. Skin-resident cells, especially keratinocytes, play essential roles in skin immunity. Damage to the integrity of the skin barrier triggers the localized release of proinflammatory factors from keratinocytes, which attract neutrophils.
View Article and Find Full Text PDFPlatelet-derived HMGB1 induces NETosis, exacerbating brain damage in the photothrombotic stroke model.
Mol Med
February 2025
Department of Anatomy, Inha University School of Medicine, Iinha 100, Nam-Gu, Inchon, 22212, Republic of Korea.
Following cerebral ischemia, neutrophil extracellular traps (NETs) contribute significantly to brain damage by exacerbating delayed immune cell infiltration and vascular injury. They are detected both in brain tissue and within blood vessels. Danger-associated molecular pattern (DAMP) molecules have been implicated in inducing NETosis after cerebral ischemia.
View Article and Find Full Text PDF"The NET effect": Neutrophil extracellular traps-a potential key component of the dysregulated host immune response in sepsis.
Crit Care
February 2025
Department of Intensive Care, Raymond Poincaré Hospital, APHP University Versailles Saint Quentin-University Paris Saclay, INSERM, Garches, France.
Neutrophils release neutrophil extracellular traps (NETs) as part of a healthy host immune response. NETs physically trap and kill pathogens as well as activating and facilitating crosstalk between immune cells and complement. Excessive or inadequately resolved NETs are implicated in the underlying pathophysiology of sepsis and other inflammatory diseases, including amplification of the inflammatory response and inducing thrombotic complications.
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