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Diabetic foot ulcer (DFU) requires frequent hospital visits, anti-biotic therapies, and surgical procedures. Not only this approach has debilitating consequences for patients and enormous costs for the health care system, but it is often not sufficient to prevent lower limb amputation. The immunological response in wound healing is mainly orchestrated by recruited monocytes and skin macrophages. The current hypothesis is that hyperglycaemia sustains an activated macrophages’ phenotype that inhibits wound healing. However, well controlled diabetes is not associated with better healing, and not all the diabetic patients develop chronic foot ulcers. In this project, we aim to characterize the immunological response of patients with DFU to discover new therapeutic targets for the treatment of chronic wounds. We suggest that an altered metabolic local environment can re-program monocytes/macrophages towards dysfunctional phenotypes unable to accomplish the healing process. Here, by using a longitudinal study cohort combined with clinical information, transcriptomic and proteomic analysis at single cell level, we will characterize the landscape of monocytes/macrophage populations involved in healing, and non-healing, foot ulcers.  Functional validation  will be performed in human skin organoids.   My group´s unique access to patient material combined with cutting-edge methodologies provides an exceptional platform to identify genes and pathways involved in chronic DFU.