ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
CCR2+ Ly6C(hi) inflammatory monocyte recruitment exacerbates acute disability following intracerebral hemorrhage.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 2 of them syntheses that pooled it.
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Who cites it
134 citing papers in PubMed, 2 syntheses or guidelines pooled it, 232 citations in OpenAlex.
- Association between circulating inflammatory biomarkers and functional outcome or perihaematomal oedema after ICH: a systematic review & meta-analysis.Wellcome open research · 2023Pooled it
- Prognostic impact of leukocytosis in intracerebral hemorrhage: A PRISMA-compliant systematic review and meta-analysis.Medicine · 2019Pooled it
- Hematoma Interleukin-1 Receptor Antagonist Concentrations Predict Long-Term Outcome in Acute Human Intracerebral Hemorrhage.Annals of neurology · 2026Trial
- Monocyte-to-high-density lipoprotein cholesterol ratio predicts hematoma expansion and poor outcomes in patients with spontaneous intracerebral hemorrhage.BMC neurology · 2026Article
- Remodelin treatment reshapes inflammation-related transcriptomic signatures in experimental thalamic hemorrhage.Frontiers in genetics · 2026Article
- Early CCR2-dependent monocyte recruitment defines a critical neuroinflammatory window after subarachnoid hemorrhage.Frontiers in immunology · 2026Article
- Intraparenchymal B cell therapy protects neurological function and modulates local neuroinflammation in experimental hemorrhagic stroke.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Ovarian cancer drives TLR5-dependent expansion of myeloid progenitors through systemic ligand dissemination.Journal of leukocyte biology · 2025Article
- Peripheral monocyte count is associated with hematoma clearance after intracerebral hemorrhage: a multicenter retrospective study.Neurosurgical review · 2025Article
- Review
- Injury to repair: Functions of microglia and monocyte-derived cells in ischemic stroke.Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association · 2025Review
- Research Progress on the Relationship Between the Intestinal Barrier and Macrophages.Current issues in molecular biology · 2025Review
- Interleukin-1 regulates myeloid cell trafficking and cerebral blood flow following intracerebral haemorrhage.Disease models & mechanisms · 2025Article
- Neutrophil degranulation is increased at seven days after human intracerebral hemorrhage, but not at 72 h, and correlates with decreased miR-3613 and miR-3690.BMC neurology · 2025Article
- CXCR3-mediated natural killer cell infiltration exacerbates white matter injury after intracerebral haemorrhage.Brain : a journal of neurology · 2025Article
- Pro-repair macrophages driven by CGRP rescue white matter integrity following intracerebral hemorrhage.Journal of neuroinflammation · 2025Article
- The spatiotemporal transcriptional profiling of murine brain during cerebral malaria progression and after artemisinin treatment.Nature communications · 2025Article
- Role of Regulatory T Cells in Intracerebral Hemorrhage.Molecular neurobiology · 2025Review
- Stroke-induced neuroplasticity in spiny mice in the absence of tissue regeneration.NPJ Regenerative medicine · 2024Article
- Immunomodulation by the combination of statin and matrix-bound nanovesicle enhances optic nerve regeneration.NPJ Regenerative medicine · 2024Article
74 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Intracerebral hemorrhage (ICH) is a devastating type of stroke that lacks a specific treatment. An intense immune response develops after ICH, which contributes to neuronal injury, disability, and death. However, the specific mediators of inflammation-induced injury remain unclear. The objective of the present study was to determine whether blood-derived CCR2+ Ly6C(hi) inflammatory monocytes contribute to disability. ICH was induced in mice and the resulting inflammatory response was quantified using flow cytometry, confocal microscopy, and neurobehavioral testing. Importantly, blood-derived monocytes were distinguished from resident microglia by differential CD45 staining and by using bone marrow chimeras with fluorescent leukocytes. After ICH, blood-derived CCR2+ Ly6C(hi) inflammatory monocytes trafficked into the brain, outnumbered other leukocytes, and produced tumor necrosis factor. Ccr2(-/-) mice, which have few circulating inflammatory monocytes, exhibited better motor function following ICH than control mice. Chimeric mice with wild-type CNS cells and Ccr2(-/-) hematopoietic cells also exhibited early improvement in motor function, as did wild-type mice after inflammatory monocyte depletion. These findings suggest that blood-derived inflammatory monocytes contribute to acute neurological disability. To determine the translational relevance of our experimental findings, we examined CCL2, the principle ligand for the CCR2 receptor, in ICH patients. Serum samples from 85 patients were collected prospectively at two hospitals. In patients, higher CCL2 levels at 24 h were independently associated with poor functional outcome at day 7 after adjusting for potential confounding variables. Together, these findings suggest that inflammatory monocytes worsen early disability after murine ICH and may represent a therapeutic target for patients.
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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.