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Mycolactone cytotoxicity in Schwann cells could explain nerve damage in Buruli ulcer

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 t...

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Detalles Bibliográficos
Autores principales: En, Junichiro, Kitamoto, Sho, Kawashima, Akira, Yonezawa, Suguru, Kishi, Yoshito, Ishii, Norihisa, Goto, Masamichi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5559071/
https://www.ncbi.nlm.nih.gov/pubmed/28783752
http://dx.doi.org/10.1371/journal.pntd.0005834
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author En, Junichiro
Kitamoto, Sho
Kawashima, Akira
Yonezawa, Suguru
Kishi, Yoshito
Ishii, Norihisa
Goto, Masamichi
author_facet En, Junichiro
Kitamoto, Sho
Kawashima, Akira
Yonezawa, Suguru
Kishi, Yoshito
Ishii, Norihisa
Goto, Masamichi
author_sort En, Junichiro
collection PubMed
description 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.
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spelling pubmed-55590712017-08-25 Mycolactone cytotoxicity in Schwann cells could explain nerve damage in Buruli ulcer En, Junichiro Kitamoto, Sho Kawashima, Akira Yonezawa, Suguru Kishi, Yoshito Ishii, Norihisa Goto, Masamichi PLoS Negl Trop Dis Research Article 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. Public Library of Science 2017-08-04 /pmc/articles/PMC5559071/ /pubmed/28783752 http://dx.doi.org/10.1371/journal.pntd.0005834 Text en © 2017 En et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
En, Junichiro
Kitamoto, Sho
Kawashima, Akira
Yonezawa, Suguru
Kishi, Yoshito
Ishii, Norihisa
Goto, Masamichi
Mycolactone cytotoxicity in Schwann cells could explain nerve damage in Buruli ulcer
title Mycolactone cytotoxicity in Schwann cells could explain nerve damage in Buruli ulcer
title_full Mycolactone cytotoxicity in Schwann cells could explain nerve damage in Buruli ulcer
title_fullStr Mycolactone cytotoxicity in Schwann cells could explain nerve damage in Buruli ulcer
title_full_unstemmed Mycolactone cytotoxicity in Schwann cells could explain nerve damage in Buruli ulcer
title_short Mycolactone cytotoxicity in Schwann cells could explain nerve damage in Buruli ulcer
title_sort mycolactone cytotoxicity in schwann cells could explain nerve damage in buruli ulcer
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5559071/
https://www.ncbi.nlm.nih.gov/pubmed/28783752
http://dx.doi.org/10.1371/journal.pntd.0005834
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