Abstract 707: Cortical-bone Stem Cell Therapy Alters the Inflammatory Response After Myocardial Infarction

Abstract

Ischemic heart diseases like myocardial infarction are the largest contributors to cardiovascular disease world-wide. The resulting cardiac cell death impairs function of the heart and can lead to heart failure and death. Re-perfusion of the ischemic tissue is necessary but causes damage to the surrounding tissue by re-perfusion injury and initiates a sterile inflammatory response. Cortical bone stem cells (CBSCs) have been shown to increase pump function and decrease scar size in a large animal swine model of myocardial infarction. To explore the potential cause of these changes, we hypothesized that CBSCs were altering the inflammatory response after re-perfusion thereby changing the wound healing process. To test this, we performed serial immune cell analysis of the blood and tissue from Gottingen mini-swine that underwent 90 minutes of lateral anterior descending coronary artery ischemia followed by 7 days of re-perfusion to assess changes in immune cell recruitment and phenotype. Our findings indicate that CBSCs modify the cytokines released by immune cells in the infarct, decrease macrophage infiltration of the infarct 3 days after MI, and increase the recruitment of CD4+ T-cells to the infarct zone 7 days after MI. In addition, these changes reflect a pro-healing inflammatory environment. From this data, we conclude that CBSCs are influencing immune cell recruitment dynamics and phenotype, and these changes may contribute to the decreased scar size and increased pump function seen in CBSC-treated animals.