The necrotic subcutaneous tissue of the Buruli lesions can be extensive. Wound healing is a major issue in Buruli ulcer and healing rates can range widely between patients, although it is not clear why. Haemostatic components including thrombomodulin have known roles in wound healing, therefore this research will throw light onto these under-explored areas. This is a collaborative study with the University of Surrey (UK) and sponsored by a Wellcome Trust grant to Dr Rachel Simmonds. The overarching hypothesis is that disordered haemostasis in the skin tissue of BU patients initiates lesion formation and determines clinical susceptibility.  Here we at explore that role of haemostasis (blood clotting) in the pathogenesis of Buruli ulcer.

This study will substantially increase our understanding of the pathogenic mechanism of Buruli ulcer lesion development. It will show whether it might be possible to improve BU treatment strategies by harnessing anticoagulants alongside antibiotics to reduce healing times. It will contribute to knowledge of the interaction between coagulation and infectious diseases more widely.

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