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在心肌梗塞后,心周脂肪组织调节颗粒形成,纤维化和心脏功能

Michael Horckmans¹, Mariaelvy Bianchini², Donato Santovito²

¹Brussels, Belgium (M.H., J.-Y.S., I.N.).

|November 24, 2017

概括

在心肌梗塞 (MI) 后,心周脂肪组织 (AT) 含有激活免疫细胞的淋巴群. 这种协调影响心脏炎症和结果, 揭示了心脏病发作的新机制.

科学领域:

免疫学
心脏病学
脂肪组织生物学

背景情况:

心周脂肪组织 (AT) 含有密集的淋巴细胞群.
这些淋巴细胞在心肌梗塞后的炎症和心脏结局中的作用尚不清楚.

研究的目的:

调查心脏AT淋巴群在心脏病发作后的炎症反应中的作用.
确定这些聚合物对心脏功能和心肌纤维化后的影响.

主要方法:

在人类和小鼠冠状动脉疾病和心脏病发作模型中检查心周AT淋巴群.
使用B细胞枯竭,颗粒细胞巨细胞殖民地刺激因子 (GM-CSF) 阻断和CCR7缺乏的小鼠来评估免疫细胞的流通和功能.
通过流细胞计量量化白细胞,并通过组织学和心声学评估心脏纤维化和心室功能.

主要成果:

在患有冠状动脉疾病的患者和心脏病发作的小鼠中观察到更大的B细胞和增加的GM-CSF产生B细胞.
激活的树突细胞 (DCs) 从心脏病发作迁移到心周AT,促进T细胞扩张.
在特定模型中,心脏AT操纵 (B细胞枯竭,GM-CSF阻塞或AT去除) 调节了免疫细胞反应,减少了心脏中性粒细胞透,并改善了心脏功能.

结论:

在心脏病发作后,心周AT作为关键的免疫枢纽协调炎症反应.
这种机制涉及淋巴细胞群,B细胞和迁移的DCs,影响颗粒形成和心脏结果.
针对心脏AT免疫功能可能为心脏病发作后的恢复提供治疗策略.

关键词:

乙淋巴细胞树突细胞颗粒细胞-巨细胞殖民地刺激因子造血干细胞淋巴细胞组织干细胞

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