Myocardial infarction (MI) wound healing is accomplished through scar formation initiated by an acute inflammatory response. The post-MI inflammatory phase is marked by a dramatic recruitment of neutrophils to the heart where they become activated. Studies within the clinic have demonstrated that increased quantities of circulating neutrophils serve as a predictor of death and adverse prognoses. Studies have demonstrated that elimination of this neutrophil response prior to MI delays scar formation and contributes to worsening heart failure. These two narratives indicate that although increased quantities of neutrophils may contribute to pathogenesis of heart failure, a certain number are required for appropriate scar formation. Either side of this balance could contribute to worsened cardiac function. Due to their short lifespan, the body must maintain the number of circulating neutrophils through steady-state granulopoiesis. However, in circumstances of immune challenge (such as in MI), the enhanced demand for neutrophil production is met through a reactive process known as emergency granulopoiesis. Whether or not neutrophils produced through emergency granulopoiesis exhibit different character or function has not been investigated previously and presents a gap in current understanding. Additionally, how any altered neutrophil function may contribute to the pathogenesis of heart failure post-MI is unknown. We hypothesize that neutrophils produced via emergency granulopoiesis exhibit altered functions which contribute to the pathogenesis of heart failure. This project seeks to determine if emergency granulopoiesis produces neutrophils with aberrant secretory function and if emergency granulopoiesis contributes to post-MI heart failure. The objectives of the proposed research are 1) to determine if MI-induced emergency granulopoiesis gives rise to neutrophils with differential functionality and 2) to determine if emergency granulopoiesis delays scar formation and contributes to heart failure post-MI. Successful completion of the proposed research will contribute to the knowledge of neutrophil function in situations of inflammatory stress such as after MI and the role of neutrophils in post-MI scar formation. Additionally, identification of differential functions and their role in the pathogenesis of heart failure could present avenues of study for future identification of therapeutic targets facilitating post-MI recovery.