Objectives: The mechanisms for the beneficial impact of bone marrow cell (BMC) therapy after myocardial infarction (MI) are ill-defined. We hypothesized that the implanted cells improve function by attenuating post-MI inflammation and repair. Methods: In mice, 3x10⁵ fresh bone marrow cells were implanted immediately after coronary ligation. Cardiac function was evaluated over time. Inflammatory cytokines and cells were measured, and their impacts on the (myo)fibroblastic repair response, angiogenesis, and scar formation were determined. All differences below had a P<0.05. Results: BMC implantation reduced the decline in fractional shortening and ventricular dilation. Invasive hemodynamics confirmed a difference in systolic function at day 7 and diastolic function at day 28 favoring the BMC group. Interestingly, BMC implantation caused a 1.6-fold increase in number of macrophages infiltrating the infarct but did not affect neutrophils. This increase was associated with a 1.9-fold higher myocardial TNF The heightened inflammatory response was associated with a 1.4-fold induction of TGF and 1.3-fold induction of bFGF. These changes resulted in a 1.6-fold increase in SMA and a 1.9-fold increase in total DDR2 expressing cells in the BMC group. These two markers are expressed by cardiac (myo)fibroblasts. Capillary density in the borderzone increased 2.0-fold. Consistent with a more robust repair-mediated scar 'contracture', the final scar size was 0.7-fold smaller in the BMC group. Conclusions: After MI, bone marrow cell therapy induced a more robust inflammatory response which improved the 'priming' of the (myo)fibroblast repair phase. Enhancing this response may further improve the beneficial impact of cellular therapy.