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Publication : Eosinophils improve cardiac function after myocardial infarction.

First Author  Liu J Year  2020
Journal  Nat Commun Volume  11
Issue  1 Pages  6396
PubMed ID  33328477 Mgi Jnum  J:301420
Mgi Id  MGI:6504611 Doi  10.1038/s41467-020-19297-5
Citation  Liu J, et al. (2020) Eosinophils improve cardiac function after myocardial infarction. Nat Commun 11(1):6396
abstractText  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.
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