Eosinophils improve cardiac function after myocardial infarction

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 Diederichsen, Lars M. Rasmussen, Dazhu Li, Gail Newton, Francis W. Luscinskas, Lijun Liu, Peter Libby, Jing Wang (), Junli Guo () and Guo-Ping Shi ()
Additional contact information
Jing Liu: Brigham and Women’s Hospital and Harvard Medical School
Chongzhe Yang: Brigham and Women’s Hospital and Harvard Medical School
Tianxiao Liu: Brigham and Women’s Hospital and Harvard Medical School
Zhiyong Deng: Brigham and Women’s Hospital and Harvard Medical School
Wenqian Fang: Brigham and Women’s Hospital and Harvard Medical School
Xian Zhang: Brigham and Women’s Hospital and Harvard Medical School
Jie Li: Brigham and Women’s Hospital and Harvard Medical School
Qin Huang: Brigham and Women’s Hospital and Harvard Medical School
Conglin Liu: Brigham and Women’s Hospital and Harvard Medical School
Yunzhe Wang: Brigham and Women’s Hospital and Harvard Medical School
Dafeng Yang: Brigham and Women’s Hospital and Harvard Medical School
Galina K. Sukhova: Brigham and Women’s Hospital and Harvard Medical School
Jes S. Lindholt: Odense University Hospital
Axel Diederichsen: Odense University Hospital
Lars M. Rasmussen: Odense University Hospital
Dazhu Li: Huazhong University of Science and Technology
Gail Newton: Brigham and Women’s Hospital and Harvard Medical School
Francis W. Luscinskas: Brigham and Women’s Hospital and Harvard Medical School
Lijun Liu: University of Toledo
Peter Libby: Brigham and Women’s Hospital and Harvard Medical School
Jing Wang: Peking Union Medical College
Junli Guo: Brigham and Women’s Hospital and Harvard Medical School
Guo-Ping Shi: Brigham and Women’s Hospital and Harvard Medical School

Nature Communications, 2020, vol. 11, issue 1, 1-15

Abstract: Abstract 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.

Date: 2020
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DOI: 10.1038/s41467-020-19297-5

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