Mycobacterium ulcerans is the causative agent of the chronic skin infection Buruli ulcer. In contrast to most mycobacteria, M. ulcerans is predominantly found in the extracellular milieu in patient lesions. This is attributed to the production of a polyketide lactone, mycolactone, which inhibits innate immune responses and is cytotoxic to macrophages. Nevertheless, early in infection, intracellular bacteria are readily detectable and genetic evidence suggests that macrophages may play a role in controlling disease progression. In particular, polymorphisms in components of the autophagy pathway are reported to influence the severity of Buruli ulcer. However, little is known about the interaction between M. ulcerans and macrophages. We are currently investigating the cellular response to M. ulcerans by the autophagy pathway in macrophages. Early findings indicate that autophagy markers are upregulated in infected THP-1 macrophage-like cells, but these rarely colocalise with the bacteria.