Maruša Rihar, Rajia Bahri, Vida Forstnerič, Silvia Bulfone-Paus, Peter Korošec
{"title":"肥大细胞、嗜碱性细胞和内皮细胞之间CCL2/ C-C趋化因子受体2型介导的相互作用","authors":"Maruša Rihar, Rajia Bahri, Vida Forstnerič, Silvia Bulfone-Paus, Peter Korošec","doi":"10.1002/clt2.70044","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Background</h3>\n \n <p>IL-33 is involved in allergic processes by promoting the release of various mast cell (MC) chemokines, including CCL2. However, it is yet unclear which specific cell type is primarily responsible for producing CCL2 during acute allergic reactions. This study aims to investigate the role of IL-33 in promoting CCL2 production in mast cells and assess the effect of MC-derived CCL2 on basophil migration and endothelial permeability.</p>\n </section>\n \n <section>\n \n <h3> Methods</h3>\n \n <p>Human blood-derived MCs (hMCs) were generated from peripheral blood precursors, passively sensitized with IgE, treated with IL-33, and stimulated with anti-IgE. The concentrations of nine cytokines known to influence immune cell chemotaxis (CCL2, CCL5, CCL11, MIP-1α, IL-8, IL-10, IL-13, granulocyte-macrophage colony-stimulating factor (GM-CSF), and vascular endothelial growth factor (VEGF) were assessed in the supernatants of hMCs. Subsequently, we investigated the impact of MC-derived CCL2 on basophil migration in vitro, as well as its effect on endothelial monolayer permeability using human umbilical vein endothelial cells (HUVECs).</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>Stimulation with anti-IgE induced a significant release of CCL2, GM-CSF, IL-8 and VEGF from hMCs. Additionally, incubation with IL-33 overnight increased the production of several cytokines. Mast cell-derived CCL2 not only enhanced basophil migration in vitro but also increased endothelial monolayer permeability in HUVECs. The effect was reversed by a C–C chemokine receptor type 2 (CCR2) antagonist, indicating the involvement of CCL2 signaling through the CCR2 receptor.</p>\n </section>\n \n <section>\n \n <h3> Conclusions</h3>\n \n <p>IL-33 induces the production of chemotactic cytokines in hMCs. Mast cell-derived CCL2 plays an important role in basophil chemotaxis in vitro and affects endothelial monolayer permeability in the HUVEC model.</p>\n </section>\n </div>","PeriodicalId":10334,"journal":{"name":"Clinical and Translational Allergy","volume":"15 2","pages":""},"PeriodicalIF":4.6000,"publicationDate":"2025-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/clt2.70044","citationCount":"0","resultStr":"{\"title\":\"CCL2/C–C chemokine receptor type 2-mediated interactions among mast cells, basophils, and endothelial cells\",\"authors\":\"Maruša Rihar, Rajia Bahri, Vida Forstnerič, Silvia Bulfone-Paus, Peter Korošec\",\"doi\":\"10.1002/clt2.70044\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n \\n <section>\\n \\n <h3> Background</h3>\\n \\n <p>IL-33 is involved in allergic processes by promoting the release of various mast cell (MC) chemokines, including CCL2. However, it is yet unclear which specific cell type is primarily responsible for producing CCL2 during acute allergic reactions. This study aims to investigate the role of IL-33 in promoting CCL2 production in mast cells and assess the effect of MC-derived CCL2 on basophil migration and endothelial permeability.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Methods</h3>\\n \\n <p>Human blood-derived MCs (hMCs) were generated from peripheral blood precursors, passively sensitized with IgE, treated with IL-33, and stimulated with anti-IgE. The concentrations of nine cytokines known to influence immune cell chemotaxis (CCL2, CCL5, CCL11, MIP-1α, IL-8, IL-10, IL-13, granulocyte-macrophage colony-stimulating factor (GM-CSF), and vascular endothelial growth factor (VEGF) were assessed in the supernatants of hMCs. Subsequently, we investigated the impact of MC-derived CCL2 on basophil migration in vitro, as well as its effect on endothelial monolayer permeability using human umbilical vein endothelial cells (HUVECs).</p>\\n </section>\\n \\n <section>\\n \\n <h3> Results</h3>\\n \\n <p>Stimulation with anti-IgE induced a significant release of CCL2, GM-CSF, IL-8 and VEGF from hMCs. Additionally, incubation with IL-33 overnight increased the production of several cytokines. Mast cell-derived CCL2 not only enhanced basophil migration in vitro but also increased endothelial monolayer permeability in HUVECs. The effect was reversed by a C–C chemokine receptor type 2 (CCR2) antagonist, indicating the involvement of CCL2 signaling through the CCR2 receptor.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Conclusions</h3>\\n \\n <p>IL-33 induces the production of chemotactic cytokines in hMCs. 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CCL2/C–C chemokine receptor type 2-mediated interactions among mast cells, basophils, and endothelial cells
Background
IL-33 is involved in allergic processes by promoting the release of various mast cell (MC) chemokines, including CCL2. However, it is yet unclear which specific cell type is primarily responsible for producing CCL2 during acute allergic reactions. This study aims to investigate the role of IL-33 in promoting CCL2 production in mast cells and assess the effect of MC-derived CCL2 on basophil migration and endothelial permeability.
Methods
Human blood-derived MCs (hMCs) were generated from peripheral blood precursors, passively sensitized with IgE, treated with IL-33, and stimulated with anti-IgE. The concentrations of nine cytokines known to influence immune cell chemotaxis (CCL2, CCL5, CCL11, MIP-1α, IL-8, IL-10, IL-13, granulocyte-macrophage colony-stimulating factor (GM-CSF), and vascular endothelial growth factor (VEGF) were assessed in the supernatants of hMCs. Subsequently, we investigated the impact of MC-derived CCL2 on basophil migration in vitro, as well as its effect on endothelial monolayer permeability using human umbilical vein endothelial cells (HUVECs).
Results
Stimulation with anti-IgE induced a significant release of CCL2, GM-CSF, IL-8 and VEGF from hMCs. Additionally, incubation with IL-33 overnight increased the production of several cytokines. Mast cell-derived CCL2 not only enhanced basophil migration in vitro but also increased endothelial monolayer permeability in HUVECs. The effect was reversed by a C–C chemokine receptor type 2 (CCR2) antagonist, indicating the involvement of CCL2 signaling through the CCR2 receptor.
Conclusions
IL-33 induces the production of chemotactic cytokines in hMCs. Mast cell-derived CCL2 plays an important role in basophil chemotaxis in vitro and affects endothelial monolayer permeability in the HUVEC model.
期刊介绍：
Clinical and Translational Allergy, one of several journals in the portfolio of the European Academy of Allergy and Clinical Immunology, provides a platform for the dissemination of allergy research and reviews, as well as EAACI position papers, task force reports and guidelines, amongst an international scientific audience.
Clinical and Translational Allergy accepts clinical and translational research in the following areas and other related topics: asthma, rhinitis, rhinosinusitis, drug hypersensitivity, allergic conjunctivitis, allergic skin diseases, atopic eczema, urticaria, angioedema, venom hypersensitivity, anaphylaxis, food allergy, immunotherapy, immune modulators and biologics, animal models of allergic disease, immune mechanisms, or any other topic related to allergic disease.
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