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Eosinophils improve cardiac function after myocardial infarction

2020; Nature Portfolio; Volume: 11; Issue: 1 Linguagem: Inglês

10.1038/s41467-020-19297-5

2041-1723

Jing Liu, Chongzhe Yang, Tianxiao Liu, Zhiyong Deng, Wenqian Fang, Xian Zhang, Jie Li, Qin Huang, Conglin Liu, Yunzhe Wang, Dafeng Yang, Galina K. Sukhova, Jes S. Lindholt, Axel Cosmus Pyndt Diederichsen, Lars Melholt Rasmussen, Dazhu Li, Gail Newton, Francis W. Luscinskas, Lijun Liu, Peter Libby, Jing Wang, Junli Guo, Guo‐Ping Shi,

Heart Failure Treatment and Management

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-β-induced cardiac fibroblast Smad2/3 activation, and TNF-α-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.