ArticleClinical and experimental immunology2009
Differences in virulence and immune response induced in a murine model by isolates of Mycobacterium ulcerans from different geographic areas.
Article in Clinical and experimental immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 27 citations in OpenAlex.
- Levels of pathogen virulence and host resistance both shape the antibody response to an emerging bacterial disease.Scientific reports · 2021Article
- Vaccine-Specific Immune Responses against Mycobacterium ulcerans Infection in a Low-Dose Murine Challenge Model.Infection and immunity · 2020Article
- Microdeletion on chromosome 8p23.1 in a familial form of severe Buruli ulcer.PLoS neglected tropical diseases · 2018Article
- Global and local environmental changes as drivers of Buruli ulcer emergence.Emerging microbes & infections · 2017Review
- Evaluating decontamination protocols for the isolation of Mycobacterium ulcerans from swabs.BMC microbiology · 2017Article
- Virulence and immune response induced by Mycobacterium avium complex strains in a model of progressive pulmonary tuberculosis and subcutaneous infection in BALB/c mice.Infection and immunity · 2013Article
- BCG-mediated protection against Mycobacterium ulcerans infection in the mouse.PLoS neglected tropical diseases · 2011Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Buruli ulcer (BU) is the third most common mycobacterial disease in immunocompetent hosts. BU is caused by Mycobacterium ulcerans, which produces skin ulcers and necrosis at the site of infection. The principal virulence factor of M. ulcerans is a polyketide-derived macrolide named mycolactone, which has cytotoxic and immunosuppressive activities. We determined the severity of inflammation, histopathology and bacillary loads in the subcutaneous footpad tissue of BALB/c mice infected with 11 different M. ulcerans isolates from diverse geographical areas. Strains from Africa (Benin, Ghana, Ivory Coast) induced the highest inflammation, necrosis and bacillary loads, whereas the strains collected from Australia, Asia (Japan, Malaysia, New Guinea), Europe (France) and America (Mexico) induced mild inflammation. Subsequently, animals were infected with the strain that exhibited the highest (Benin) or lowest (Mexico) level of virulence in order to analyse the local immune response generated. The Mexican strain, which does not produce mycolactone, induced a predominantly T helper type 1 (Th1) cytokine profile with constant high expression of the anti-microbial peptides beta defensins 3 and 4, in co-existence with low expression of the anti-inflammatory cytokines interleukin (IL)-10, IL-4 and transforming growth factor (TGF)-beta. The highly virulent strain from Benin which produces mycolactone A/B induced the opposite pattern. Thus, different local immune responses were found depending on the infecting M. ulcerans strain.
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