Microbial modification of macrophages to arrest phagosome maturation is generally considered an undesirable outcome in terms of host defence. However, repurposing of this process may provide a new avenue for stem cell delivery in regenerative medicine. We investigated the feasibility of creating a “macrophage shuttle” – where a modified macrophage would ingest, but not digest, one or more stem cells and then deliver these to a tissue site requiring regeneration. After obtaining ethical clearance from the Human Research Ethics Committee of Stellenbosch University, peripheral monocytes were isolated from human donor whole blood using density centrifugation. Primary monocyte cultures were maintained under normal cell culture conditions, but exposed to 50ng/ml E.coli LPS and 20ng/ml IFN-γ for 6 days to pre-differentiate them into type M1 macrophages, which have known ability to cross endothelial barriers. M1 macrophages were then treated with Wortmannin, Concanamycin A and Chloroquine to achieve phagosome maturation arrest and thus prevent digestion of stem cells after phagocytosis. For ethical reasons, blue fluorescent latex beads (diameter 6 µm) were used to simulate stem cells. These beads were opsonised by coating them with (red) Alexa Fluor 647-labelled goat anti-human IgG. This also allowed for visualisation of phagosomal digestion. Phagosomal degradation of red antibody signal and phagosome acidification (using pHrodo as indicator) was assessed visually over a period of 2 hours using confocal microscopy, as well as quantitatively by flow cytometry at 2 hours. All experiments were carried out in triplicate and repeated on three separate occasions (n=3). Results showed that phagosome maturation arrest was indeed succesful: firstly, the pH within phagosomes of modified cells was less likely to become acidic when compared to controls (40±35% vs. 92±3% of cells, t-test P<0.05). Secondly, the coated antibody was digested from latex beads in control cells to a greater extent that in modified cells (complete digestion in 7.5±3.1% vs. 1.5±1.1% of cells, P<0.05). Thirdly, macrophage modification did not compromise phagocytic capacity (successful phagocytosis in 61±16% of control cells vs. 65±13% of modified cells). Evidence of transendothelial transport of C2C12 skeletal muscle stem cells by modified macrophages will also be presented. Variability in results for phagocytic capacity and antibody digestion was similar for control and modified cells, but the extent of inhibition of phagosome acidification varied more. This variability may be ascribed to the fact that a different human monocyte donor was used for each repeat experiment and highlights the requirement for individualised medicine in this context. In conclusion, although more developmental work is required, this system presents an exciting new avenue for investigation in the fields of regenerative medicine and inflammation.