期刊
NATURE COMMUNICATIONS
卷 11, 期 1, 页码 -出版社
NATURE PORTFOLIO
DOI: 10.1038/s41467-020-19297-5
关键词
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资金
- National Natural Science Foundation of China [91939107, 81770487]
- Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences [2016-I2M-1-006, 2019-I2M-5-023]
- Open program for Key Laboratory of Emergency and Trauma of Ministry of Education Hainan Medical University [KLET-201917]
- National Institute of Health [HL080472, HL123568, HL60942, AG063839]
- RRM Charitable Fund
- American Heart Association [20POST35210968]
Clinical studies reveal changes in blood eosinophil counts and eosinophil cationic proteins that may serve as risk factors for human coronary heart diseases. Here we report an increase of blood or heart eosinophil counts in humans and mice after myocardial infarction (MI), mostly in the infarct region. Genetic or inducible depletion of eosinophils exacerbates cardiac dysfunction, cell death, and fibrosis post-MI, with concurrent acute increase of heart and chronic increase of splenic neutrophils and monocytes. Mechanistic studies reveal roles of eosinophil IL4 and cationic protein mEar1 in blocking H2O2- and hypoxia-induced mouse and human cardiomyocyte death, TGF-beta -induced cardiac fibroblast Smad2/3 activation, and TNF-alpha -induced neutrophil adhesion on the heart endothelial cell monolayer. In vitro-cultured eosinophils from WT mice or recombinant mEar1 protein, but not eosinophils from IL4-deficient mice, effectively correct exacerbated cardiac dysfunctions in eosinophil-deficient dblGATA mice. This study establishes a cardioprotective role of eosinophils in post-MI hearts. Blood eosinophil (EOS) counts may serve as risk factors for human coronary heart diseases. Here the authors show that increased circulating and myocardial EOS after myocardial infarction play a cardioprotective role by reducing cardiomyocyte death, cardiac fibroblast activation and fibrosis, and endothelium activation-mediated inflammatory cell accumulation.
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