Eotaxin-2 blockade ameliorates experimental autoimmune encephalomyelitis
Eotaxin-2 blockade ameliorates experimental autoimmune encephalomyelitis作者机构：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
出 版 物：《World Journal of Immunology》 (世界免疫学杂志)
年 卷 期：2013年第3卷第1期
页 面：7-14页
学科分类：12[管理学] 1204[管理学-公共管理] 120402[管理学-社会医学与卫生事业管理(可授管理学、医学学位)] 1004[医学-公共卫生与预防医学(可授医学、理学学位)] 10[医学]
摘 要：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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