ArticleJournal of leukocyte biology2022
Plasma extracellular vesicles released after severe burn injury modulate macrophage phenotype and function.
Article in Journal of leukocyte biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 36 citations in OpenAlex.
- Interpretable machine learning model predicts the early gastrointestinal dysfunction risk in severely burned patients: a multicenter-based study.International journal of surgery (London, England) · 2026Article
- Burn-associated metabolic dysfunction: could extracellular vesicles play a role?Clinical science (London, England : 1979) · 2026Review
- Mitochondria as a Therapeutic Target for Burn Injury.Biomolecules · 2026Review
- Enhanced Burn Wound Healing and Conversion Prevention Through Inhibition of High Mobility Group Box 1 in a Scald Burn Rat Model.Journal of burn care & research : official publication of the American Burn Association · 2026Article
- Macrophages on demand: How tissue trauma shapes their role.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2026Review
- Integrated serum metabolomics reveals severity-associated exploratory metabolic signatures in burn patients.Frontiers in physiology · 2026Article
- Retinal pigment epithelium-derived extracellular vesicles mediate outer blood retinal barrier disruption in response to AMD-related stress.Cell communication and signaling : CCS · 2025Article
- Effects of Early Stage Second-Degree Burn Blister Exudate on Macrophage Polarization andReports of biochemistry & molecular biology · 2025Article
- DAMP-driven trained immunity: metabolic and epigenetic reprogramming in critical illness and chronic inflammation.Frontiers in immunology · 2025Review
- Extracellular vesicles in burn injury: roles, mechanisms, and applications.Burns & trauma · 2025Review
- Temporal changes in the protein cargo of extracellular vesicles and resultant immune reprogramming after severe burn injury in humans and mice.Frontiers in immunology · 2025Article
- Role of oxidative stress in post-burn wound healing.Burns & trauma · 2025Review
- MULTIMODAL NUCLEAR FACTOR-ERYTHROID-2-RELATED FACTOR (NRF2) THERAPY IN THE CONTEXT OF MAMMALIAN TARGET OF RAPAMYCIN (MTOR) INHIBITION REPROGRAMS THE ACUTE SYSTEMIC AND PULMONARY IMMUNE RESPONSE AFTER COMBINED BURN AND INHALATION INJURY.Shock (Augusta, Ga.) · 2024Article
- Radiation-induced eCIRP impairs macrophage bacterial phagocytosis.Journal of leukocyte biology · 2024Article
- Evidence that keratinocyte microvesicle particles carrying platelet-activating factor mediate the widespread multiorgan damage associated with intoxicated thermal burn injury.Journal of leukocyte biology · 2024Article
- Delivery of Nitric Oxide by Chondroitin Sulfate C Increases the Rate of Wound Healing through Immune Modulation.ACS applied bio materials · 2024Article
- Development of 5-Fluorouracil/pH-Responsive Adjuvant-Embedded Extracellular Vesicles for Targeting αPharmaceutics · 2024Article
- Downregulation of HMGB1 carried by macrophage-derived extracellular vesicles delays atherosclerotic plaque formation through Caspase-11-dependent macrophage pyroptosis.Molecular medicine (Cambridge, Mass.) · 2024Article
- Nanoparticle-Based Therapeutics for Enhanced Burn Wound Healing: A Comprehensive Review.International journal of nanomedicine · 2024Review
- Involvement of extracellular vesicles in the progression, diagnosis, treatment, and prevention of whole-body ionizing radiation-induced immune dysfunction.Frontiers in immunology · 2023Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Extracellular vesicles (EVs) have emerged as key regulators of immune function across multiple diseases. Severe burn injury is a devastating trauma with significant immune dysfunction that results in an ∼12% mortality rate due to sepsis-induced organ failure, pneumonia, and other infections. Severe burn causes a biphasic immune response: an early (0-72 h) hyper-inflammatory state, with release of damage-associated molecular pattern molecules, such as high-mobility group protein 1 (HMGB1), and proinflammatory cytokines (e.g., IL-1β), followed by an immunosuppressive state (1-2+ wk post injury), associated with increased susceptibility to life-threatening infections. We have reported that early after severe burn injury HMGB1 and IL-1β are enriched in plasma EVs. Here we tested the impact of EVs isolated after burn injury on phenotypic and functional consequences in vivo and in vitro using adoptive transfers of EV. EVs isolated early from mice that underwent a 20% total body surface area burn injury (burn EVs) caused similar hallmark cytokine responses in naïve mice to those seen in burned mice. Burn EVs transferred to RAW264.7 macrophages caused similar functional (i.e., cytokine secretion) and immune gene expression changes seen with their associated phase of post-burn immune dysfunction. Burn EVs isolated early (24 h) induced MCP-1, IL-12p70, and IFNγ, whereas EVs isolated later blunted RAW proinflammatory responses to bacterial endotoxin (LPS). We also describe significantly increased HMGB1 cargo in burn EVs purified days 1 to 7 after injury. Thus, burn EVs cause immune outcomes in naïve mice and macrophages similar to findings after severe burn injury, suggesting EVs promote post-burn immune dysfunction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.