L’ulcèrede Buruli

Houngbedji, G.; Frenette, Jérôme

doi:10.1051/medsci/2011272187

Cited by 3 publications

(4 citation statements)

References 27 publications

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“…We recently showed that BU extends well beyond the skin and significantly affects underlying skeletal muscles (25)(26)(27)(28). The present study showed that WT-MU is much more cytotoxic for myoblasts, myotubes, and fully differentiated skeletal muscles than M neg -MU, indicating that the major culprit involved in muscle damage/dysfunction is mycolactone.…”

Section: Discussionsupporting

confidence: 46%

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Investigation of wild-type and mycolactone-negative mutantMycobacterium ulceranson skeletal muscle: IGF-1 protects against mycolactone-induced muscle catabolism

Dufresne

Frenette

2013

American Journal of Physiology-Regulatory, Integrative and Comp

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Dufresne SS, Frenette J. Investigation of wild-type and mycolactone-negative mutant Mycobacterium ulcerans on skeletal muscle: IGF-1 protects against mycolactone-induced muscle catabolism. Buruli ulcer (BU), which is caused by Mycobacterium ulcerans (MU), is an endemic and neglected tropical disease that affects mostly subcutaneous tissues. Skeletal muscle under infected skin is also subject to serious dysfunctions and contractures. The goal of this study was to investigate the effects of an infection with the wild-type M. ulcerans (WT-MU) or the mycolactone-negative Mycobacterium ulcerans (M neg -MU) mutant strains on myotubes or fully differentiated skeletal muscles. WT-MU infection decreased by 22% and 29% the maximal muscle force at days 7 and 42 postinfection, respectively, while M neg -MU induced no decrease at day 7 postinfection and a small but significant 13% decrease in muscle force at day 42. A 13.2-fold and 4.3-fold increase in neutrophil and macrophage concentrations, respectively, was observed on day 42 following the injection of WT-MU. However, the increases in neutrophil and macrophage concentrations were 2.4-fold and 5.5-fold in M neg -MU. Myoblast proliferation decreased by 20%, myotube diameter by 45%, MyHC levels by 32%, while MuRF-1 levels increased by 22.8% when C2C12 cells and WT-MU were cocultured for 48 h at a multiplicity of infection of 5:1. In contrast, M neg -MU had no significant effect. Interestingly, the addition of 1,000 ng/ml of IGF-1 to the WT-MU/C2C12 coculture significantly improved all of these biological parameters. The present investigation clearly established that muscle dysfunction and chronic inflammation in the presence of WT-MU are largely caused by the release of mycolactone, and the addition of recombinant IGF-1 was sufficient to alleviate some of the antiproliferative and atrophic effects of mycolactone.Buruli ulcer; insulin-like growth factor-1; muscle dysfunction; Mycobacterium ulcerans; mycolactone BURULI ULCER (BU), WHICH IS caused by Mycobacterium ulcerans (MU) infections, is a disease of wet tropical and subtropical zones and is closely related to tuberculosis and leprosy (38,47). It is widely distributed in more than 30 countries, and the rate of morbidity may surpass tuberculosis and leprosy in some endemic regions of Africa (2,49). Each year, between 5,000 and 6,000 new cases of BU are reported, and more than 50% of whom are children under 15 years of age (10, 50). Recent animal studies have shown that the BU spreads well beyond the skin and significantly affects the underlying tissues, including skeletal muscles. (25-28).Mycolactone, a macrolide toxin with highly destructive capacities, is the deleterious agent of MU. It can cause skin necrosis, cell cycle arrest, immunosuppression, cell death by apoptosis, and necrosis (19,23,36,48). Mycolactone-negative MU mutants are reportedly nonvirulent and noncytotoxic for subcutaneous tissues and leukocytes (1,8,36). Mycolactone diffuses passively through infected tissues and can rapidly penetrate cells. It enters ...

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Section: Discussionsupporting

confidence: 46%

“…WT-MU was originally isolated from a human ulcer in 2005 and was identified by RT-PCR using the specific insertion sequence IS2404 and by Ziehl-Neelsen staining (25)(26)(27)(28). M neg -MU was a spontaneous mutant isolated from nonpigmented colonies of MU 1615, a strain from Malaysia that produces mycolactone A/B (34).…”

Section: Methodsmentioning

confidence: 99%

Investigation of wild-type and mycolactone-negative mutantMycobacterium ulceranson skeletal muscle: IGF-1 protects against mycolactone-induced muscle catabolism

Dufresne

Frenette

2013

American Journal of Physiology-Regulatory, Integrative and Comp

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“…> L'ulcère de Buruli, ou infection à Mycobacterium ulcerans [11] (➜), est une maladie à tropisme esse ntiel lement cutané, qui est diagnostiquée dans 30 pays localisés principalement dans la ceinture tropicale. Cette maladie tropicale négligée et émergente représente actuellement la troisième mycobactériose la plus pré-valente chez les sujets immunocompé-tents, après la tuberculose et la lèpre.…”

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La mycolactone

et al. 2016

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“…après plusieurs semaines, en l'absence de prise en charge, les lésions évoluent en une ulcéra-tion cutanée qui reste indolore malgré une extension qui peut être importante (Figure 1). Les destructions précisément six cas d'ulcère cutané à bords décollés et met en évi-dence de nombreux bacilles acido-alcoolo-résistants (Baar) dans les tissus lésés [30]. Leur isolement est difficile.…”

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