CXCL1 and myocardial infarction: EOS genetic deficiency or antibody-mediated EOS depletion worsened the cardiac functions post-MI along with increased infarct size and myocardium fibrosis, reduced myocardium Th2 cytokines (IL4, IL10, and IL13), and increased myocardium chemokine C-X-C motif ligands (CXCL1 and CXCL2) and inflammatory cells (neutrophils and macrophages) at 4 days post-MI.