ArticleAtherosclerosis2017
Oxidized LDL activated eosinophil polarize macrophage phenotype from M2 to M1 through activation of CD36 scavenger receptor.
Article in Atherosclerosis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 56 citations in OpenAlex.
- Foam cells: tracing the diverse cellular origins and their linked signaling pathways.Journal of translational medicine · 2025Review
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- Differential roles of eosinophils in cardiovascular disease.Nature reviews. Cardiology · 2025Review
- Protective effect ofFood & nutrition research · 2025Article
- Eosinophil specialization is regulated by exposure to the esophageal epithelial microenvironment.Journal of leukocyte biology · 2024Article
- Eosinophils in Colorectal Cancer: Emerging Insights into Anti-Tumoral Mechanisms and Clinical Implications.International journal of molecular sciences · 2024Review
- Identification of crucial genes that induce coronary atherosclerosis through endothelial cell dysfunction in AMI-identifying hub genes by WGCNA.American journal of translational research · 2022Article
- Cyclin D1b induces changes in the macrophage phenotype resulting in promotion of tumor metastasis.Experimental biology and medicine (Maywood, N.J.) · 2021Article
- Theranostic nanoplatform to target macrophages enables the inhibition of atherosclerosis progression and fluorescence imaging of plaque in ApoE(-/-) mice.Journal of nanobiotechnology · 2021Article
- Inflammation in Metabolic and Cardiovascular Disorders-Role of Oxidative Stress.Life (Basel, Switzerland) · 2021Review
- Immunological mechanisms underlying sterile inflammation in the pathogenesis of atherosclerosis: potential sites for intervention.Expert review of clinical immunology · 2021Review
- Eosinophil Deficiency Promotes Aberrant Repair and Adverse Remodeling Following Acute Myocardial Infarction.JACC. Basic to translational science · 2020Article
- Type-I interferons in atherosclerosis.The Journal of experimental medicine · 2020Review
- APE1 inhibits foam cell formation from macrophages via LOX1 suppression.American journal of translational research · 2020Article
- Adipose Tissue Immunomodulation: A Novel Therapeutic Approach in Cardiovascular and Metabolic Diseases.Frontiers in cardiovascular medicine · 2020Review
- Contributions of innate type 2 inflammation to adipose function.Journal of lipid research · 2019Review
- CD36 tango in cancer: signaling pathways and functions.Theranostics · 2019Review
- CD 36: Focus on Epigenetic and Post-Transcriptional Regulation.Frontiers in genetics · 2019Review
- Melittin Induced G1 Cell Cycle Arrest and Apoptosis in Chago-K1 Human Bronchogenic Carcinoma Cells and Inhibited the Differentiation of THP-1 Cells into Tumour- Associated MacrophagesAsian Pacific journal of cancer prevention : APJCP · 2018Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND AND
aimsInflammation, particularly innate immunity, plays an important role in cardiovascular diseases. The aim of this study was to investigate whether atherogenic determinants such as oxidized LDL modulate the phenotype of eosinophils.
methodsCultured eosinophils were treated with oxidized LDL and the expression of selective inflammatory and anti-inflammatory cytokines was determined. In addition, the eosinophil receptor and signaling that mediate these events were identified.
resultsTreatment of cultured eosinophils with oxidized LDL (Ox-LDL) specifically induced the expression of IFNα and IFNβ without affecting expression of other proinflammatory cytokines, such as TNFα, IL-1β, and IL-6. In macrophages, Ox-LDL downregulated expression of both IFNα and IFNβ, suggesting that the effect of Ox-LDL on the expression of type I interferons is specific to eosinophils. Furthermore, we noted that eosinophils constitutively expressed IL-4 and IL-13, and Ox-LDL markedly downregulated their expression. Analysis of Ox-LDL signaling revealed that eosinophils constitutively expressed SRB2, CD36, and CD68 scavenger receptors, and Ox-LDL markedly induced the expression of CD36. Further analysis of CD36 signaling by siRNA and neutralizing antibodies showed that the induction of type I IFN by Ox-LDL is mediated by CD36 signaling whereas downregulation of IL-4 is independent of CD36 activation. We further showed that peritoneal macrophages treated with condition medium collected from Ox-LDL treated eosinophils markedly induced the expression of M1 markers such as iNOS, IL6, SOSC3 and TNFα whereas the condition medium from non-treated eosinophils significantly induced expression of M2 markers like ARG1 and CCL24.
conclusionsOur data suggest that an atherogenic condition could activate eosinophils and modulate the phenotype of macrophages (from M2 to M1 phenotype), in part, through the CD36 receptor signaling.
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