ArticleCell death & disease2024
Chemerin attracts neutrophil reverse migration by interacting with C-C motif chemokine receptor-like 2.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
18 citing papers in PubMed.
- Novel Adipokines in Critical Illness and Sepsis: Chemerin, Vaspin, and Omentin-1: A Comprehensive Evidence-Based Review.Biomedicines · 2026Review
- Clitocine suppresses TNBC progression by boosting CCRL2 to block survival signals and neutrophil-driven inflammation.Journal of biological engineering · 2026Article
- Metabolic Mechanisms of Neutrophil Phagocytic Activity in Patients with Widespread Purulent Peritonitis Bacterial Peritonitis Before and After Surgery.International journal of molecular sciences · 2026Article
- New Insights Into the Role of Neutrophils in Lymphoma.Cancer medicine · 2026Review
- Chemical and Mechanical Regulation of Leukocyte Migration.Cold Spring Harbor perspectives in biology · 2026Review
- Dysregulation of Neutrophil-Endothelial Communication in Sepsis: Mechanisms and Therapeutic Perspectives.Cells · 2026Review
- Regulated Release of Small Extracellular Vesicles Directs Neutrophil Recruitment in Cutaneous Wound Healing.The Journal of investigative dermatology · 2026Article
- Chemerin/ChemerinR1 axis and inflammation-related diseases.Frontiers in molecular biosciences · 2026Review
- Neutrophil Irg1/itaconate axis protects against experimental colitis by suppressing local inflammation and maintaining hematopoietic homeostasis.Molecular biomedicine · 2025Article
- Innate immune cross-talk: The central role of neutrophils and macrophages in ANCA-associated vasculitis.Molecular biology of the cell · 2025Review
- The role of neutrophils in the pathophysiology of inflammatory bowel diseases.Periodontology 2000 · 2025Review
- The Role of Chemerin in Neutrophil Activation and Diseases of the Lung.Biomedicines · 2025Review
- Adipokines: masterminds of metabolic inflammation.Nature reviews. Immunology · 2025Review
- Dengue virus infection: how platelet-leukocyte crosstalk shapes thrombotic events and inflammation.Molecular biology reports · 2025Review
- Ginsenoside Rh2-Pretreated Mesenchymal Stem Cell Exosomes Ameliorate Collagen-Induced Arthritis via N6-Methyladenosine Methylation.Biomaterials research · 2025Article
- Identification and validation of key biomarkers of the glycolysis-ketone body metabolism in heart failure based on multi-omics and machine learning.Frontiers in cardiovascular medicine · 2025Article
- Chemokines in the resolution of inflammation: key players and targets for therapeutic modulation.Frontiers in immunology · 2025Review
- Chemerin in the Spotlight: Revealing Its Multifaceted Role in Acute Myocardial Infarction.Biomedicines · 2024Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Neutrophil reverse migration (rM) is a recently identified phenomenon in which neutrophils migrate away from the inflammatory site back into the vasculature following initial infiltration, which involved in the resolution of loci inflammatory response or dissemination of inflammation. Present study was aimed to explore the mechanisms in neutrophil rM. By scRNA-seq on the white blood cells in acute lung injury model, we found rM-ed neutrophils exhibited increased gene expression of C-C motif chemokine receptor-like 2 (Ccrl2), an atypical chemokine receptor. Furthermore, an air pouch model was established to directly track rM-ed neutrophils in vivo. Air pouches were generated by 3 ml filtered sterile air injected subcutaneously for 3 days, and then LPS (2 mg/kg) was injected into the pouches to mimic the inflammatory state. For the rM-ed neutrophil tracking system, cell tracker CMFDA were injected into the air pouch to stain the inflammatory loci cells, and after 6 h, stained cells in blood were regarded as the rM-ed neutrophil. Based on this tracking system, we confirmed that rM-ed neutrophils showed increased CCRL2. We also found that the concentrations of the CCRL2 ligand chemerin in plasma was increased in the late stage. Neutralizing chemerin decreased the rM-ed neutrophil ratio in the blood. These results suggest that circulating chemerin attracts neutrophils to leave inflammatory sites by interacting with CCRL2, which might involve in the dissemination of inflammation.
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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.