ArticleIn vivo (Athens, Greece)
Membrane Active Immunomodulator As a Novel Therapy for an Infectious Bacterial Disease, Buruli Ulcer.
Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- Article
- Recent Advances in the Management Strategies for Buruli Ulcers.Pathogens (Basel, Switzerland) · 2023Review
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimMycobacterium ulcerans causes the necrotizing skin disease Buruli ulcer (BU), characterized by the formation of subcutaneous lesions and immunosuppression thought to be mediated by the virulence factor mycolactone. Since early BU lesions are typically painless, patients often seek standard oral antibiotic therapy at the advanced stages when the treatment is less effective. Given that currently there is no curative topical treatment for BU, our objective was to evaluate a plasma membrane fluidizer, diethyl azelate (DEA), as a potential novel topical therapy for BU. MATERIALS AND
methodsWe evaluated the effects of DEA against bacterial extracts and live strains of M. ulcerans ATCC 35840 (mycolactone positive; M+) and ATCC 19423 (mycolactone negative; M-) by measuring cytokine levels in cultured cells and tissue extracts using multiplexed immunoassays and numbers of skin lesions as the endpoints.
resultsIn vitro, DEA counteracted immunosuppression induced by extract from the M+ strain in the 3-D human skin model (EpiDerm) and in human dendritic cells. In vivo, topical DEA reduced immunosuppressive activities of M+ and M- strains at all stages of BU, including advanced ulcers. DEA also diminished lesion formation and ulceration, accelerated healing of skin lesions and preserved normal immune responsiveness to pathogen-associated molecular pattern receptor agonists in blood of infected animals.
conclusionThe efficacy of DEA in BU models is linked to overcoming the immunosuppressive activity of virulence factors produced by M. ulcerans. Thanks to its pluripotent activity, DEA is a promising novel treatment for BU and possibly other pathogenic mycobacteria.
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