ArticlePediatric research2023
CCL3 aggravates intestinal damage in NEC by promoting macrophage chemotaxis and M1 macrophage polarization.
Article in Pediatric research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 21 citations in OpenAlex.
- Identification and validation of a robust inflammation-related three-gene signature for the diagnosis of neonatal necrotizing enterocolitis via machine learning integration.Pediatric surgery international · 2026Article
- Identification of diagnostic biomarkers for neonatal necrotizing enterocolitis via machine learning screening and single-cell virtual gene knockout validation.Journal of cell communication and signaling · 2026Article
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- Integrated multi-omics analysis reveals dendritic cell centered regulatory networks and therapeutic targets in necrotizing enterocolitis.Frontiers in immunology · 2026Article
- GSDMD deficiency attenuates BPD by suppressing macrophage pyroptosis and promoting M2 polarization.Cell death discovery · 2025Article
- Research Progress on the Relationship Between the Intestinal Barrier and Macrophages.Current issues in molecular biology · 2025Review
- GSDMD deficiency mitigates intestinal damage via macrophage pyroptosis control in experimental NEC.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Identification and Exploration of Pyroptosis-Related Genes in Macrophage Cells Reveal Necrotizing Enterocolitis Heterogeneity Through Single-Cell and Bulk-Sequencing.International journal of molecular sciences · 2025Article
- Targeted delivery of CCL3 reprograms macrophage antigen presentation and enhances the efficacy of immune checkpoint blockade therapy in hepatocellular carcinoma.Journal for immunotherapy of cancer · 2025Article
- CCL3 as a novel biomarker in the diagnosis of necrotizing enterocolitis.BMC pediatrics · 2024Article
- Time-resolved scRNA-seq reveals transcription dynamics of polarized macrophages with influenza A virus infection and antigen presentation to T cells.Emerging microbes & infections · 2024Article
- Iron Oxide Nanoparticles Engineered Macrophage-Derived Exosomes for Targeted Pathological Angiogenesis Therapy.ACS nano · 2024Article
- Design, fabrication and clinical characterization of additively manufactured tantalum hip joint prosthesis.Regenerative biomaterials · 2024Article
- Acute and chronic impact of interleukin-33 stimulation on chemokines and growth factors in human cord blood-derived mast cells.PloS one · 2024Article
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- Glutamine coated titanium for synergistic sonodynamic and photothermal on tumor therapy upon targeted delivery.Frontiers in bioengineering and biotechnology · 2023Article
- Cellular and transcriptome signatures unveiled by single-cell RNA-Seq followingFrontiers in immunology · 2023Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNEC is a life-threatening gastrointestinal disease in neonates, the pathogenesis of which remains poorly understood.
methodsCCL3 levels in intestinal tissue of mice were measured and analyzed. HE staining was used to assess pathological changes in intestinal tissue. FCM was used to detect the proportion and phenotype of macrophages. RNA-seq and RT-PCR were used to evaluate the effect of CCL3 on macrophages.
resultsCCL3 was highly expressed in the intestinal tissues of mice with NEC and induced macrophage infiltration. Transcriptome data showed that CCL3 strongly induced a transition in the phenotype of macrophages into a proinflammatory one. Mechanistically, in vivo experiments confirmed that CCL3 induced M1 macrophage polarization in NEC intestinal tissue, thereby aggravating inflammatory injury of intestinal tissue, which was alleviated by anti-CCL3 treatment. In addition, in vitro experiments showed that CCL3 significantly enhances the expression of M1-related genes in both PMφ and BMDM while inhibiting the expression of M2-related genes, which was also alleviated by anti-CCl3 treatment.
conclusionsOur data elucidated the involvement of CCL3 in the pathogenesis of NEC, in which upregulated CCL3 expression exacerbated inflammatory intestinal damage by regulating macrophage chemotaxis and M1 phenotype polarization, suggesting that blocking CCL3 may be a potential strategy for effective intervention in NEC. IMPACT: Our study represents an important conceptual advancement that CCL3 may be one of the key culprits of intestinal tissue damage in patients with NEC. CCL3 aggravates inflammatory intestinal injury and intestinal mucosal barrier imbalance by regulating the chemotaxis, polarization, and function of macrophages. Blocking CCL3 significantly reduced NEC-mediated intestinal injury, suggesting a new potential therapeutic strategy.
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