ArticleInfection and immunity2007
Mycolactone-mediated inhibition of tumor necrosis factor production by macrophages infected with Mycobacterium ulcerans has implications for the control of infection.
Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 94 citations in OpenAlex.
- Clinical efficacy of combination of rifampin and streptomycin for treatment of Mycobacterium ulcerans disease.Antimicrobial agents and chemotherapy · 2010Trial
- Review
- Inflammasome-triggered IL-18 controls skin inflammation in the progression of Buruli ulcer.PLoS pathogens · 2023Article
- The One That Got Away: How Macrophage-Derived IL-1β Escapes the Mycolactone-Dependent Sec61 Blockade in Buruli Ulcer.Frontiers in immunology · 2021Article
- Mycolactone toxin induces an inflammatory response by targeting the IL-1β pathway: Mechanistic insight into Buruli ulcer pathophysiology.PLoS pathogens · 2020Article
- Vaccine-Specific Immune Responses against Mycobacterium ulcerans Infection in a Low-Dose Murine Challenge Model.Infection and immunity · 2020Article
- Antimicrobial activity of Mycobacteriophage D29 Lysin B during Mycobacterium ulcerans infection.PLoS neglected tropical diseases · 2019Article
- Recombinant Antibodies against Mycolactone.Toxins · 2019Article
- Phage therapy as a renewed therapeutic approach to mycobacterial infections: a comprehensive review.Infection and drug resistance · 2019Article
- The potent effect of mycolactone on lipid membranes.PLoS pathogens · 2018Article
- Infiltrating leukocytes surround early Buruli ulcer lesions, but are unable to reach the mycolactone producing mycobacteria.Virulence · 2017Article
- Mycolactone reveals the substrate-driven complexity of Sec61-dependent transmembrane protein biogenesis.Journal of cell science · 2017Article
- Mechanistic insights into the inhibition of Sec61-dependent co- and post-translational translocation by mycolactone.Journal of cell science · 2016Article
- Genetic Variation in Autophagy-Related Genes Influences the Risk and Phenotype of Buruli Ulcer.PLoS neglected tropical diseases · 2016Article
- Interferon-γ Is a Crucial Activator of Early Host Immune Defense against Mycobacterium ulcerans Infection in Mice.PLoS neglected tropical diseases · 2016Article
- Clinical Features of Spontaneous Partial Healing During Mycobacterium ulcerans Infection.Open forum infectious diseases · 2016Article
- Bacterial Toxins as Pathogen Weapons Against Phagocytes.Frontiers in microbiology · 2016Review
- Spontaneous Healing of Mycobacterium ulcerans Lesions in the Guinea Pig Model.PLoS neglected tropical diseases · 2015Article
- Recombinant BCG Expressing Mycobacterium ulcerans Ag85A Imparts Enhanced Protection against Experimental Buruli ulcer.PLoS neglected tropical diseases · 2015Article
- Mycolactone-Dependent Depletion of Endothelial Cell Thrombomodulin Is Strongly Associated with Fibrin Deposition in Buruli Ulcer Lesions.PLoS pathogens · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenicity of Mycobacterium ulcerans, the agent of Buruli ulcer, depends on the cytotoxic exotoxin mycolactone. Little is known about the immune response to this pathogen. Following the demonstration of an intracellular growth phase in the life cycle of M. ulcerans, we investigated the production of tumor necrosis factor (TNF) induced by intramacrophage bacilli of diverse toxigenesis/virulence, as well as the biological relevance of TNF during M. ulcerans experimental infections. Our data show that murine bone marrow-derived macrophages infected with mycolactone-negative strains of M. ulcerans (nonvirulent) produce high amounts of TNF, while macrophages infected with mycolactone-positive strains of intermediate or high virulence produce intermediate or low amounts of TNF, respectively. These results are in accordance with the finding that TNF receptor P55-deficient (TNF-P55 KO) mice are not more susceptible than wild-type mice to infection by the highly virulent strains but are more susceptible to nonvirulent and intermediately virulent strains, demonstrating that TNF is required to control the proliferation of these strains in animals experimentally infected by M. ulcerans. We also show that mycolactone produced by intramacrophage M. ulcerans bacilli inhibits, in a dose-dependent manner, but does not abrogate, the production of macrophage inflammatory protein 2, which is consistent with the persistent inflammatory responses observed in experimentally infected mice.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.