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Anti eotaxin-2 antibodies attenuate the initiation and progression of experimental atherosclerosis

World Journal of Cardiovascular Diseases 2013年第4期3卷 339-346页

作者： Adi Mor Arnon Afek michal entin-meer Gad Keren Jacob George ChemomAb Ltd. Tel Aviv Israel The Department of Cardiology Tel Aviv Sourasky Medical Center Tel Aviv Israel

Background: The chemokine eotaxin-2 is a potent chemoattractant for inflammatory cells, the predominants of which are eosinophils. Human and murine atherosclerotic plaques are known to exhibit inflammatory phenotypes where a complex interaction of cytokine and chemokines plays a role. We tested the hypothesis that eotaxin-2 (eo-2) plays a causative role in the initiation and progression of experimental atherosclerosis. Methods and Results: Sera collected from atherosclerotic ApoE knockout (KO) mice, exhibited significantly higher levels of eo-2 compared to sera collected from their background age matched C57BL/6 litters by ELISA. Moreover, levels of eo-2 were higher in old atherosclerotic ApoE KO mice than in young animals. Similarly, the expression level of the eo-2 receptor, CCR3, was increased in splenocytes of old ApoE compared to the young littermates. Administration of polyclonal blocking antibodies to eotaxin-2 resulted in a significant reduction of early atherosclerotic plaques in ApoE KO mice whereas prolonged treatment of mice with advanced plaques led to atheroma stabilization. A monoclonal antibody (D8) prepared against eo-2 attenuated adhesion of lymphocytes to fibronectin and potently inhibited their migration towards VEGF. Monoclonal blocking antibodies to eo-2 also significantly reduced atherosclerotic plaques in ApoE KO mice. Conclusion: Eo-2 serum levels are elevated in sera of ApoE KO mice with experimental atherosclerosis and its blockade is associated with reduced fatty streak accumulation and increased plaque stabilization.

关键词： Atherosclerosis Vulnerable Plaque Inflammation Eotaxin-2 Chemokines

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Eotaxin-2 blockade ameliorates experimental autoimmune encephalomyelitis

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World Journal of Immunology 2013年第1期3卷 7-14页

作者： Karin Mausner-Fainberg Arnon Karni Jacob George michal entin-meer Arnon Afek Department of Neurology The Neuroimmunology Laboratory64239 Tel Aviv Israel Sackler’s Medical School Tel Aviv University 64239 Tel Aviv Israel Department of Cardiology Kaplan Medical CenterRehovot 64239 Tel Aviv Israel Department of Cardiology TASMC 64239 Tel Aviv Israel Sheba Medical Center Tel Hashomer 52621 Ramat Gan Israel

AIM: To study the effect of blocking the eo-2 pathwayon the development and severity of experimental autoimmune encephalomyelitis(EAE). METHODS: We produced m Ab directed against eo-2,named D8. MOG35-55 induced-EAE mice were dailyintravenously injected with either 25 μg or 100 μg D8,or with vehicle control alone [phosphate-buffered saline(PBS)], starting from day 0 post immunization and weremonitored for EAE clinical score(n = 10 in each group).Mice were sacrificed on day 58 and their sera were assessed for the presence of anti-myelin oligodendrocyteglycoprotein(anti-MOG) antibodies autoantibodies, aswell as for the profile of pro-inflammatory cytokines andchemokines. Histological analysis of brain sections wasperformed by hematoxylin and eosin ***: Daily treatment of EAE induced mice with D8 significantly decreased the severity of EAE symptoms. Treatment with both concentrations of D8 ameliorated EAE symptoms compared to PBS treated mice, starting from day 42 post immunization(0.89 ± 0.35 in D8 25 μg and D8 100 μg treated groups vs 2.11 ± 0.38 in the PBS treated group, P = 0.03). A significant improvement in EAE clinical score compared to total Ig G treated mice was observed with the higher concentration of D8(0.81 ± 0.38 in D8 100 μg treated group vs 2.11 ± 0.31 in Ig G1 treated group, on day 56 post immunization, P = 0.04). D8 treated mice with EAE did not significantly exhibit lower sera levels of anti-MOG autoantibodies compared to Ig G-treated mice. However, they expressed lower sera levels of the pro-inflammatory cytokines: tumor necrosis factor(7.8 ± 0.2 pg/m L in D8 100 μg treated mice vs 19.9 ± 3.4 pg/m L in Ig G treated mice, P = 0.005) and interferon-gamma(1.4 ± 0.6 pg/m L in D8 100 μg treated mice vs 3.6 ± 0.4 pg/m L in Ig G treated mice, P = 0.02), as well as reduced levels of the chemokine macrophage chemoattractant protein-1(27.2 ± 3.1 pg/m L in D8 100 μg treated mice vs 63.7 ± 12.3 pg/m L in Ig G treated mice, P = 0.03). These findings

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