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抑制 Bcl2L12 可减轻心脏嗜酸性粒细胞相关炎症。

Inhibition of Bcl2L12 Attenuates Eosinophilia-Related Inflammation in the Heart.

机构信息

State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Research Center of Allergy & Immunology, Shenzhen University School of Medicine, Shenzhen, China.

出版信息

Front Immunol. 2020 Sep 11;11:1955. doi: 10.3389/fimmu.2020.01955. eCollection 2020.

DOI:10.3389/fimmu.2020.01955
PMID:33013849
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7516035/
Abstract

The eosinophilic inflammation plays a critical role in myocarditis (Mcd); its underlying mechanism remains to be further elucidated. This study aims to investigate the role of Bcl2-like protein 12 (Bcl2L12) in inducing the defects of apoptosis in eosinophils (Eos) of the heart tissues. Human explant heart samples were collected. Eosinophilia and myocarditis (Mcd)-like inflammation were induced in the mouse heart by immunizing with murine cardiac α-myosin heavy chain (MyHCα) peptides. Markedly more Eos were observed in heart tissues from patients with Mcd than those from patients with dilated cardiomyopathy. Eos isolated from Mcd hearts showed the signs of apoptosis defects. The Eo counts in the Mcd heart tissues were positively correlated with the Bcl2L12 expression in Eos isolated from the heart tissues. Exposure to interleukin 5 in the culture induced the expression of Bcl2L12 in Eos. Bcl2L12 bound c-Myc, the transcription factor of Fas ligand (FasL), to prevent c-Myc from binding to the FasL promoter, to restrict the FasL gene transcription in Eos. Inhibition of Bcl2L12 prevented the induction of eosinophilia and Mcd-like inflammation in the mouse heart. The Bcl2L12 expression contributes to apoptosis defects in Eos of the Mcd heart. Blocking Bcl2L12 prevents the eosinophilia induction and alleviates Mcd-like inflammation in mice.

摘要

嗜酸性粒细胞炎症在心肌炎 (Mcd) 中发挥着关键作用；其潜在机制仍有待进一步阐明。本研究旨在探讨 Bcl2 样蛋白 12 (Bcl2L12) 在诱导心脏组织中嗜酸性粒细胞 (Eos) 凋亡缺陷中的作用。

收集人类心脏标本。通过用鼠心肌α肌球蛋白重链 (MyHCα) 肽免疫小鼠，诱导嗜酸性粒细胞增多和类似心肌炎 (Mcd) 的炎症。与扩张型心肌病患者相比，Mcd 患者心脏组织中观察到的嗜酸性粒细胞明显更多。从 Mcd 心脏中分离出的嗜酸性粒细胞表现出凋亡缺陷的迹象。Mcd 心脏组织中的嗜酸性粒细胞计数与从心脏组织中分离出的嗜酸性粒细胞中 Bcl2L12 的表达呈正相关。在培养物中暴露于白细胞介素 5 会诱导嗜酸性粒细胞中 Bcl2L12 的表达。Bcl2L12 结合 c-Myc，即 Fas 配体 (FasL) 的转录因子，以防止 c-Myc 与 FasL 启动子结合，从而限制嗜酸性粒细胞中 FasL 基因的转录。抑制 Bcl2L12 可防止小鼠心脏中嗜酸性粒细胞增多和类似 Mcd 的炎症的诱导。Bcl2L12 的表达导致 Mcd 心脏中嗜酸性粒细胞的凋亡缺陷。阻断 Bcl2L12 可防止嗜酸性粒细胞增多，并缓解 Mcd 样炎症在小鼠中的发生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dd9/7516035/9a831bcc07ff/fimmu-11-01955-g0007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dd9/7516035/9a831bcc07ff/fimmu-11-01955-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dd9/7516035/de32a17b328b/fimmu-11-01955-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dd9/7516035/0e10a7da1514/fimmu-11-01955-g0002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dd9/7516035/36a44e99e928/fimmu-11-01955-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dd9/7516035/9a831bcc07ff/fimmu-11-01955-g0007.jpg

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