ArticleJournal of molecular and cellular cardiology2020
Exogenous IL-4 shuts off pro-inflammation in neutrophils while stimulating anti-inflammation in macrophages to induce neutrophil phagocytosis following myocardial infarction.
Article in Journal of molecular and cellular cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses that pooled it.
What it found
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Who cites it
44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 57 citations in OpenAlex.
- Role of Macrophages in Cardiac Remodeling: Cues From Zebrafish Heart.Immunity, inflammation and disease · 2026Pooled it
- Cardiac repair after myocardial infarction: A two-sided role of inflammation-mediated.Frontiers in cardiovascular medicine · 2022Pooled it
- Trial
- Spatiotemporal Nanotherapy After Myocardial Infarction: Targeting the Inflammatory-to-reparative Transition With Extracellular Vesicles and Engineered Nanoparticles.Cardiovascular drugs and therapy · 2026Review
- IL-15 aggravates cardiac ischemic injury via impairing macrophage efferocytosis and driving inflammation.Journal of Zhejiang University. Science. B · 2026Article
- A reparative neutrophil subpopulation accelerates spinal cord regeneration in zebrafish by controlling macrophage inflammation via Il-4.Journal of neuroinflammation · 2026Article
- Type 2 immune history imprints local training in nerve and airway associated interstitial macrophages (NAMs) for disease tolerance during lethal respiratory viral infection.Research square · 2026Article
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- Mesenchymal stromal cells modulate neutrophil phenotype via paracrine signals.Stem cell research & therapy · 2025Article
- Bioactive compounds in the modulation of oxidative stress in monocytes and macrophages.Scientific reports · 2025Article
- Exogenous Ubiquitin Differentially Modulates the Phenotype and Function of M1 and M2 Macrophages.Cells · 2025Article
- Cytokine and Oxidative Stress Imbalances in Relation to Complex Coronary Lesions in Elderly Patients.Current vascular pharmacology · 2025Article
- Immune in myocardial ischemia/reperfusion injury: potential mechanisms and therapeutic strategies.Frontiers in immunology · 2025Review
- Ischemia Reperfusion Injury Induced Systemic Inflammatory Response Following Interspecies Liver Transplantation.Hepatic medicine : evidence and research · 2025Article
- TheScience translational medicine · 2024Article
- Global IL4Rα blockade exacerbates heart failure after an ischemic event in mice and humans.American journal of physiology. Heart and circulatory physiology · 2024Observational
- IL-13 promotes functional recovery after myocardial infarction via direct signaling to macrophages.JCI insight · 2024Article
- ASO-mediated knockdown or kinase inhibition ofMolecular therapy. Nucleic acids · 2023Article
- Paracrine Responses of Cardiosphere-Derived Cells to Cytokines and TLR Ligands: A Comparative Analysis.International journal of molecular sciences · 2023Article
- IL-4 and IL-13 induce equivalent expression of traditional M2 markers and modulation of reactive oxygen species in human macrophages.Scientific reports · 2023Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
introductionMacrophages and neutrophils are primary leukocytes involved in the inflammatory response to myocardial infarction (MI). While interleukin (IL)-4 is an in vitro anti-inflammatory stimulus, the MI myocardium does not express a considerable amount of IL-4 but does express IL4 receptors. We hypothesized that continuous exogenous IL-4 infusion starting 24 h after MI would promote a polarization switch in inflammatory cells towards a reparative phenotype.
methodsC57BL/6J male mice (3-6 months of age) were subcutaneously infused with either saline (n = 17) or IL-4 (20 ng/g/day; n = 17) beginning 24 h after MI and evaluated at MI day 3.
resultsMacrophages and neutrophils were isolated ex vivo from the infarct region and examined. Exogenous IL-4 decreased pro-inflammatory Ccl3, Il12a, Tnfa, and Tgfb1 in neutrophils and increased anti-inflammatory Arg1 and Ym1 in macrophages (all p < .05). Tissue clearance by IL-4 treated neutrophils was not different, while selective phagocytosis of neutrophils doubled in IL-4 treated macrophages (p < .05). Of 24,339 genes examined by RNA-sequencing, 2042 genes were differentially expressed in macrophages from IL-4 stimulated infarct (all FDR p < .05). Pdgfc gene expression was ranked first, increasing 3-fold in macrophages stimulated with IL-4 (p = 1 × 10
conclusionsOur results indicate that exogenous IL-4 promotes inflammation resolution by turning off pro-inflammation in neutrophils while stimulating anti-inflammation in macrophages to mediate removal of apoptotic neutrophils.
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Registered trials
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