ArticleThe Journal of surgical research2009
Norepinephrine-mediated suppression of phagocytosis by wound neutrophils.
Article in The Journal of surgical research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 36 citations in OpenAlex.
- Multimodal Imaging Reveals Rapid Catecholamine Uptake and Release by Neutrophils.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Axonal regeneration and hyperglycemia in wound healing: a review on the role of activin A, TNFRSF10B, and Synaptophysin.Molecular biology reports · 2026Review
- Recent advances in the role of neuroregulation in skin wound healing.Burns & trauma · 2025Review
- Octopamine modulates the innate immune response inFrontiers in immunology · 2025Article
- Sympathetic System in Wound Healing: Multistage Control in Normal and Diabetic Skin.International journal of molecular sciences · 2023Review
- Regulation of Lysozyme Activity by Human HormonesIranian biomedical journal · 2023Article
- Effects of anti-inflammatory drugs on the expression of tryptophan-metabolism genes by human macrophages.Journal of leukocyte biology · 2018Article
- Adrenergic Signaling: A Targetable Checkpoint Limiting Development of the Antitumor Immune Response.Frontiers in immunology · 2018Review
- α-Synuclein and Noradrenergic Modulation of Immune Cells in Parkinson's Disease Pathogenesis.Frontiers in neuroscience · 2018Review
- Leukocytosis and high hematocrit levels during abdominal attacks of hereditary angioedema.BMC gastroenterology · 2013Article
- Article
- Ghrelin-mediated sympathoinhibition and suppression of inflammation in sepsis.American journal of physiology. Endocrinology and metabolism · 2012Review
- An improved cell isolation method for flow cytometric and functional analyses of cutaneous wound leukocytes.Journal of immunological methods · 2011Article
- Tumor necrosis factor and norepinephrine lower the levels of human neutrophil peptides 1-3 secretion by mixed synovial tissue cultures in osteoarthritis and rheumatoid arthritis.Arthritis research & therapy · 2010Article
- Norepinephrine represses the expression of toxA and the siderophore genes in Pseudomonas aeruginosa.FEMS microbiology letters · 2009Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe systemic response to injury is characterized by massive release of norepinephrine (NE) into the circulation as a result of global sympathetic activation. Multiple authors have demonstrated NE-mediated alterations in migration of circulating neutrophils to wounds. We hypothesized that NE further alters wound neutrophil phagocytic function through adrenergic signaling pathways.
methodsA standard subcutaneous sponge wound model was used. Murine wound neutrophils were harvested at 24 and 120 h after injury and treated with physiological (10(-9) M) and pharmacologic (10(-6) M) doses of NE. Phagocytosis of green fluorescent protein-labeled Escherichia coli was assayed by flow cytometry. The signaling pathways mediating NE modulation of phagocytosis by wound neutrophils were defined by pharmacologic manipulation of alpha- and beta-adrenoreceptors and protein kinase A.
resultsPharmacologic-dose NE, but not-physiological-dose NE, suppressed the phagocytic efficiency of 120-h wound neutrophils. This alteration in phagocytic efficiency appears to be mediated through alpha- and beta- adrenoreceptors and downstream protein kinase A. Phagocytosis by 24-h wound neutrophils was not impacted by NE treatment.
conclusionsThe present study is the first to demonstrate NE-mediated alterations in the process of phagocytosis by wound neutrophils. We conclude that NE plays a temporally and dose-defined immunomodulatory role in cutaneous wound healing through alterations in phagocytosis by wound neutrophils and may represent a target for therapeutic manipulation of the innate immune response.
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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.