Abstract
Buruli ulcer is a chronic painless skin disease caused by Mycobacterium ulcerans. The local nerve damage induced by M. ulcerans invasion is similar to the nerve damage evoked by the injection of mycolactone in a Buruli ulcer mouse model. In order to elucidate the mechanism of this nerve damage, we tested and compared the cytotoxic effect of synthetic mycolactone A/B on cultured Schwann cells, fibroblasts and macrophages. Mycolactone induced much higher cell death and apoptosis in Schwann cell line SW10 than in fibroblast line L929. These results suggest that mycolactone is a key substance in the production of nerve damage of Buruli ulcer.
Highlights
IntroductionThe disease is basically characterized by the ulcer without pain [1], but some pain is noted at the wound care dressing service [2]
Buruli ulcer is a disease characterized by the painless nature of its lesion
Buruli ulcer is a chronic skin disease caused by Mycobacterium ulcerans, and the disease is characterized by the painless nature of its lesion
Summary
The disease is basically characterized by the ulcer without pain [1], but some pain is noted at the wound care dressing service [2]. These studies suggest that Buruli ulcer lesions are initially painless, but the patients experience pain after chemotherapy, probably due to nerve regeneration. Studies of the pathological mechanism have revealed that local nerves are invaded and damaged by the causative agent, M. ulcerans [3], and that similar nerve damage is evoked by the injection of mycolactone in a mouse model [4] In both instances, Schwann cells, which play the major role in maintaining nerve function, showed vacuolar degeneration. Nerve damage was histopathologically confirmed in human Buruli ulcer lesions [5]
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