Expression data from adult left ventricular heart tissue of hypereosinophilic mice and controls

Hypereosinophilic syndrome is a progressive disease with extensive eosinophilia that results in organ damage. Patients suffer from frequent cardiac pathologies and a high mortality rate. A better understanding of the mechanisms of eosinophil-mediated tissue damage would benefit the development of new therapies. Here, we describe the cardiac pathologies that develop in a mouse model of hypereosinophilic syndrome. These IL-5 transgenic mice exhibited decreased left ventricular function already at a young age. Cardiac function worsened with age and heart weight increased. Moreover, hypereosinophilic mice developed different pathologies of the cardiac conductive system, including 2nd degree atrioventricular block and atrioventricular reentry. Cardiomyocytes from IL-5 transgenic mice showed reduced contractility. Despite immune infiltrates in the lungs, doppler echocardiography revealed no signs of pulmonary hypertension in these mice. Mechanistically, we demonstrated eosinophil infiltration of the heart tissue that lead to an inflammatory environment. Eosinophils were 100-fold more abundant in the hearts of hypereosinophilic mice than controls. Gene expression signatures showed tissue damage as well as repair and remodeling processes. Our results suggest that hypereosinophilia leads to infiltration of the heart tissue by eosinophils and tissue damage. The ongoing remodeling and repair processes are insufficient or maladapted to maintain heart function resulting in progressive deterioration. We examine expression data from three biological replicates each of left ventricular heart tissue of naïve wildtype controls, IL-5 transgenic (NJ.1638), and IL-5 transgenic ddblGATA1 mice, a total of nine mice. IL-5 transgenic mice develop hypereosinophilia and often die prematurely. We looked at cardiac gene expression to explore mechansims of cardiac pathology. Il-5 transgenic ddblGATA1 mice are included as a control with high IL-5 levels but no eosinophils.