ArticleJCI insight2019
Complement receptor C3aR1 controls neutrophil mobilization following spinal cord injury through physiological antagonism of CXCR2.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 99 citations in OpenAlex.
- Lesion level and severity acutely influence metabolomic profiles in spinal cord injury.Journal of neuropathology and experimental neurology · 2026Article
- Sex-dependent effects of peptidylarginine deiminases on neutrophil function and long-term outcomes after spinal cord injury.Experimental neurology · 2025Article
- F-box/LRR-repeat protein 12 reorchestrated microglia to inhibit scarring and achieve adult spinal cord injury repair.Signal transduction and targeted therapy · 2025Article
- Recombinant human DNase treatment mitigates extracellular trap mediated damage and improves long-term recovery after spinal cord injury in male mice.Brain, behavior, and immunity · 2025Article
- Neutrophil infiltration and microglial shifts in sepsis induced preterm brain injury: pathological insights.Acta neuropathologica communications · 2025Article
- Biomimetic "Trojan Horse" Fibers Modulate Innate Immunity Cascades for Nerve Regeneration.ACS nano · 2025Article
- C3AR1 may aggravate diabetic nephropathy by mediating oxidative stress via ITGB2 regulation in renal tubular epithelial cells.PloS one · 2025Article
- Decoding neutrophil extracellular traps and key gene drivers in unexplained pregnancy loss.Frontiers in immunology · 2025Article
- The complement system in human pregnancy and preeclampsia.Frontiers in immunology · 2025Review
- Article
- Identification of pivotal genes and regulatory networks associated with atherosclerotic carotid artery stenosis based on comprehensive bioinformatics analysis and machine learning.Frontiers in pharmacology · 2024Article
- Molecular basis of anaphylatoxin binding, activation, and signaling bias at complement receptors.Cell · 2023Article
- Neutrophil biology in injuries and diseases of the central and peripheral nervous systems.Progress in neurobiology · 2023Review
- Iron induces B cell pyroptosis through Tom20-Bax-caspase-gasdermin E signaling to promote inflammation post-spinal cord injury.Journal of neuroinflammation · 2023Article
- Sex Differences in Immune Cell Infiltration and Hematuria in SCI-Induced Hemorrhagic Cystitis.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023Article
- C3aR plays both sides in regulating resistance to bacterial infections.PLoS pathogens · 2022Review
- Evolution and Targeting of Myeloid Suppressor Cells in Cancer: A Translational Perspective.Cancers · 2022Review
- Complement Receptor 3 Pathway and NMDA Receptor 2B Subunit Involve Neuropathic Pain Associated with Spinal Cord Injury.Journal of pain research · 2022Article
- Neuroinflammation, Microglia and Implications for Retinal Ganglion Cell Survival and Axon Regeneration in Traumatic Optic Neuropathy.Frontiers in immunology · 2022Review
- NLRP6 Serves as a Negative Regulator of Neutrophil Recruitment and Function DuringFrontiers in microbiology · 2022Article
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic spinal cord injury (SCI) triggers an acute-phase response that leads to systemic inflammation and rapid mobilization of bone marrow (BM) neutrophils into the blood. These mobilized neutrophils then accumulate in visceral organs and the injured spinal cord where they cause inflammatory tissue damage. The receptor for complement activation product 3a, C3aR1, has been implicated in negatively regulating the BM neutrophil response to tissue injury. However, the mechanism via which C3aR1 controls BM neutrophil mobilization, and also its influence over SCI outcomes, are unknown. Here, we show that the C3a/C3aR1 axis exerts neuroprotection in SCI by acting as a physiological antagonist against neutrophil chemotactic signals. We show that C3aR1 engages phosphatase and tensin homolog (PTEN), a negative regulator of the phosphatidylinositol 3-kinase (PI3K)/AKT pathway, to restrain C-X-C chemokine receptor type 2-driven BM neutrophil mobilization following trauma. These findings are of direct clinical significance as lower circulating neutrophil numbers at presentation were identified as a marker for improved recovery in human SCI. Our work thus identifies C3aR1 and its downstream intermediary, PTEN, as therapeutic targets to broadly inhibit neutrophil mobilization/recruitment following tissue injury and reduce inflammatory pathology.
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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.