ArticleJournal of neuroinflammation2017
NOX2 deficiency alters macrophage phenotype through an IL-10/STAT3 dependent mechanism: implications for traumatic brain injury.
Article in Journal of neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 93 citations in OpenAlex.
- Dynamic metabolic programming of monocyte-derived cells defines immunity in CNS disease.Brain : a journal of neurology · 2026Review
- Mechanisms of inflammatory response in secondary brain injury: a review of computational approaches, challenges, and future directions.Biomechanics and modeling in mechanobiology · 2026Review
- Different Immune Cells Modified With Chimeric Antigen Receptors Are Being Applied to Ovarian Cancer: Which Is the Most Effective?Cancer medicine · 2026Review
- Macrophages on demand: How tissue trauma shapes their role.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2026Review
- Cytokines and related signaling pathways in traumatic brain injury.Frontiers in immunology · 2026Review
- Epidermal growth factor receptor modulation for neural repair: Implications for neurodegenerative disease therapy.Frontiers in molecular neuroscience · 2026Review
- Integrated transcriptomic and functional analyses reveal that NOX2 inhibition rewires the inflammatory landscape of macrophages.Frontiers in immunology · 2026Article
- The NOX2-ROS-NLRP3 inflammasome axis in traumatic brain injury.Journal of neuroinflammation · 2025Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- The functions of immune system-derived miRNAs in cardiovascular diseases.Non-coding RNA research · 2025Review
- The Role of mtDNA Mutations in Atherosclerosis: The Influence of Mitochondrial Dysfunction on Macrophage Polarization.International journal of molecular sciences · 2025Review
- Immunometabolism In Brain Aging and Neurodegeneration: Bridging Metabolic Pathways and Immune Responses.Aging and disease · 2024Review
- The dichotomic role of cytokines in aging.Biogerontology · 2024Review
- Prevotella copri transplantation promotes neurorehabilitation in a mouse model of traumatic brain injury.Journal of neuroinflammation · 2024Article
- Interaction of high-fat diet and brain trauma alters adipose tissue macrophages and brain microglia associated with exacerbated cognitive dysfunction.Journal of neuroinflammation · 2024Article
- Gut Metabolites Acting on the Gut-Brain Axis: Regulating the Functional State of Microglia.Aging and disease · 2024Review
- Redox Regulation of Immunometabolism in Microglia Underpinning Diabetic Retinopathy.Antioxidants (Basel, Switzerland) · 2024Review
- Modulation of Innate Immune Memory Dynamics by Subcellular Reactive Oxygen Species.Antioxidants & redox signaling · 2023Review
- Improving outcomes in intracerebral hemorrhage through microglia/macrophage-targeted IL-10 delivery with phosphatidylserine liposomes.Biomaterials · 2023Article
- Inhibition of NADPH Oxidase (NOX) 2 Mitigates Colitis in Mice with Impaired Macrophage AMPK Function.Biomedicines · 2023Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundNADPH oxidase (NOX2) is an enzyme system that generates reactive oxygen species (ROS) in microglia and macrophages. Excessive ROS production is linked with neuroinflammation and chronic neurodegeneration following traumatic brain injury (TBI). Redox signaling regulates macrophage/microglial phenotypic responses (pro-inflammatory versus anti-inflammatory), and NOX2 inhibition following moderate-to-severe TBI markedly reduces pro-inflammatory activation of macrophages/microglia resulting in concomitant increases in anti-inflammatory responses. Here, we report the signaling pathways that regulate NOX2-dependent macrophage/microglial phenotype switching in the TBI brain.
methodsBone marrow-derived macrophages (BMDMs) prepared from wildtype (C57Bl/6) and NOX2 deficient (NOX2
resultsUsing an LPS/IL-4-stimulated BMDM model that mimics the mixed pro- and anti-inflammatory responses observed in the injured cortex, we show that NOX2
conclusionsThese studies indicate that following TBI NOX2 inhibition promotes a robust anti-inflammatory response in macrophages/microglia that is mediated by the IL-10/STAT3 signaling pathway. Thus, therapeutic interventions that inhibit macrophage/microglial NOX2 activity may improve TBI outcomes by not only limiting pro-inflammatory neurotoxic responses, but also enhancing IL-10-mediated anti-inflammatory responses that are neuroprotective.
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