Changes in blood eosinophil levels and eosinophil cationic proteins have been discovered in clinical research to be risk factors for human coronary heart disease. Following Myocardial Infarction (MI), we found an increase in blood or heart eosinophil counts in humans and animals, particularly in the infarct zone. Post-MI cardiac dysfunction, cell death, and fibrosis are exacerbated by genetic or inducible eosinophil depletion, which is accompanied with an immediate increase in heart and a chronic rise in splenic neutrophils and monocytes. Mechanistic studies show that eosinophil IL4 and the cationic protein mEar1 play a role in preventing H2O2- and hypoxia-induced cardiomyocyte death in mice and humans, as well as TGF-induced cardiac fibroblast Smad2/3 activation and TNF-induced neutrophil adhesion on the heart endothelial cell monolayer. In vitro-cultured eosinophils from WT mice or recombinant mEar1 protein efficiently cure aggravated cardiac dysfunctions in eosinophil-deficient dblGATA mice, but not eosinophils from IL4-deficient animals. Eosinophils play a cardioprotective role in post-MI hearts, according to this study.
