Mesenchymal stem cells (MSC) are ideal candidates for stem cell-based therapies of vascular inflammation. They are progenitor cells that can replace damaged cells and they can modulate immune response cells. MSC from bone marrow and adipose tissue regulate inflammation by promoting the switch of macrophage cell from an inflammatory to an anti-inflammatory phenotype. Much less is known about the tissue resident MSC’s and their interaction with macrophage cells. We hypothesized that aortaderived mesenchymal stem cells (mAo MSC) would also promote the expression of the antiinflammatory phenotype among macrophage cells. The interaction of mAo MSC with the macrophage was examined by co-culturing the cells and exposing them to the inflammatory mediator, lipopolysaccharide (LPS). A bone marrow derived MSC cell line was used as a control. Nitric oxide (NO) and the tumor necrosis factor-α (TNFα) and interleukin-12 (IL-12) cytokines were measured using Griess reaction and ELISA assay respectively. The impact of the interaction on phagocytosis was measured using zymosan-A. We found that bone marrow derived MSC, when in co-culture with macrophage cells, performed as expected and suppressed NO, TNFα, and IL-12 production. Unexpectedly, the mAo MSC enhanced NO and TNFα production by the macrophage cells, which is indicative of the inflammatory phenotype; IL-12 production by macrophage remained unchanged. Macrophage cell phagocytic activity was significantly increased by contact with mAo MSC, which represents enhancement of the anti-inflammatory phenotype.