Monocytes are circulating innate immune cells that are known to be recruited to sites of infection. However what monocytes do at sites of infection, i.e., their function is less clear. In this thesis, I have used a low-dose foreign body Staphylococcus aureus (S. aureus) skin infection model using agar beads as a carrier for S. aureus to understand the functional role of recruited monocytes. I have characterized this infection model and shown that the S. aureus bead forms biofilm in vivo that is mediated by ica-dependent biofilm formation. Monocytes were recruited to the S. aureus bead but did not contribute to bacterial clearance. Instead, monocytes were critical for tissue repair by regulating leptin-mediated angiogenesis. In the absence of monocyte recruitment, or after monocyte depletion, elevated leptin levels locally in the skin drove dysregulated angiogenesis with dysfunctional, leaky vessels which resulted in delayed healing and scar formation. Leptin acted through LepR+ endothelial cells which drove angiogenesis. Blocking leptin signalling with an antagonist blocked the dysregulated vasculature and improved healing. Ghrelin, which is known to inhibit leptin, was produced by monocytes, and monocyte-derived ghrelin was shown to be critical for mediating repair. Altogether, in this thesis, I have uncovered a novel monocyte-leptin-angiogenesis pathway critical for repair post-infection.