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Neutrophil extracellular traps (NETs) are immunogenic extracellular DNA structures that can be released by neutrophils upon a wide variety of triggers. NETs have been demonstrated to serve as an important host defense mechanism that traps and kills microorganisms. On the other hand, they have been implicated in diverse systemic autoimmune diseases. NETs are immunogenic and toxic structures that contain a pool of relevant autoantigens including anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV) and systemic lupus erythematosus (SLE). Different forms of NETs can be induced depending on the stimulus. The amount of NETs can be quantified using different techniques including measuring DNA release in supernatants, measuring DNA-complexed with NET-molecules like myeloperoxidase (MPO) or neutrophil elastase (NE), measuring the presence of citrullinated histones by fluorescence microscopy, or flow cytometric detection of NET-components which all have different features regarding their specificity, sensitivity, objectivity, and quantity. Here is a protocol to quantify ex vivo NET formation in a highly-sensitive, high-throughput manner by using three-dimensional immunofluorescence confocal microscopy. This protocol can be applied to address various research questions about NET formation and degradation in health and disease.
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http://dx.doi.org/10.3791/59150 | DOI Listing |
mBio
September 2025
The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, California, USA.
Unlabelled: Methicillin-resistant (MRSA) is a leading cause of endovascular infections, where interactions with endothelial cells play a critical role in pathogenesis. Gp05, a prophage-encoded protein, has previously been implicated in promoting antibiotic persistence by modulating MRSA cellular physiology and evading neutrophil-mediated killing. In this study, we investigated the role of Gp05 in MRSA-endothelial cell interactions, focusing on its impact on bacterial adhesion, invasion, cytotoxicity, and the host inflammatory response.
View Article and Find Full Text PDFJ Burn Care Res
September 2025
Department of Burn Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Background: Burn injuries trigger complex immune responses and gene expression changes, impacting wound healing and systemic inflammation. Understanding these changes is crucial for identifying biomarkers and therapeutic targets.
Methods: We analyzed two GEO datasets (wound tissue (GSE8056) and blood (GSE37069)) to identify differentially expressed genes (DEGs) in burn injury samples versus controls.
Front Immunol
September 2025
Department of Geriatrics, Jilin Geriatrics Clinical Research Center, The First Hospital of Jilin University, Changchun, Jilin, China.
Kaempferol (KMF) is a dietary flavonoid exhibiting profound immunomodulatory effects across multiple immune cell populations. This review synthesizes current insights into how KMF regulates diverse immune cell populations and its therapeutic potential in inflammatory and immune-related disorders. KMF exhibits multifaceted effects on T cells.
View Article and Find Full Text PDFCardiol Cardiovasc Med
August 2025
Department of Translational Research, College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, Pomona, California 91766 USA.
Deep vein thrombosis (DVT) and pulmonary embolism (PE) are key initiating events in the development of venous thromboembolism (VTE), a condition associated with significant morbidity, mortality, and long-term complications. While traditional therapies have focused on anticoagulation and thrombolysis, current evidence describes the pivotal role of immune pathways in the pathogenesis and progression of thrombosis. This review explores the multifaceted mechanisms underlying DVT and PE, emphasizing the contribution of inflammation, leukocyte activation, and immuno-thrombosis to thrombus formation and embolization.
View Article and Find Full Text PDFJ Cereb Blood Flow Metab
September 2025
The Vivian L. Smith Department of Neurosurgery, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, USA.
Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating neurological disease, and one of the primary drivers of morbidity after aneurysm rupture is the phenomenon of delayed cerebral ischemia (DCI). Significant knowledge has been gained over the past two decades of the impact of neuroinflammation in DCI; and neutrophils are now believed to play a major role. There is significant human subject data showing the rise of neutrophil related inflammatory markers and neutrophil's association with poor outcome after aSAH, but as of yet no trials involving human subjects have been done specifically targeting neutrophils.
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