Effects of treatment with muramyl dipeptide on resistance to Mycobacterium leprae and Mycobacterium marinum infection in mice

Krahenbuhl, James L.; Humphres, R C

doi:10.1016/0162-3109(83)90048-6

Cited by 7 publications

(4 citation statements)

References 28 publications

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“…Interestingly, it has been reported that in vivo MDP treatment failed to induce resistance to Mycobacterium leprae and Mycobacterium marinum in mice (40). In addition, in vitro treatment of T cells with murabutide, an MDP analog, reversed T cell anergy to mycobacteria leprae antigens (41) suggesting that in vivo the inability to mount an effective response to muramyl dipeptide may play a role in the exacerbation of the infection.…”

Section: Discussionmentioning

confidence: 99%

Muramyl Dipeptide Induces Th17 Polarization through Activation of Endothelial Cells

Manni

Ding

Stohl

et al. 2011

The Journal of Immunology

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Endothelial cells (ECs) express the nucleotide-binding oligomerization domain (Nod) receptor 2, which recognizes the bacterial derivate muramyl dipeptide (MDP). MDP stimulation of these cells enhances their IL-6 production and may thus contribute to the immune and inflammatory activities in the skin. However, whether ECs are capable of influencing the development of T cell priming and its polarization remains unknown. We report that in vitro the murine bEnd.3 EC line induces, following MDP stimulation, a Th17 polarization at the expense of Th1 and Th2 polarization in the setting of Langerhans cell (LC) Ag presentation to responsive T cells as assessed by IL-17, IL-6, IFN-γ, and IL-4 production. Interestingly, IL-22 production, which has been associated with Th17 priming, was not influenced by MDP-treated bEnd.3 cells, illustrating differential regulation of this cytokine from IL-17. Additional analysis confirmed a significantly increased percentage of IL-17+CD4+ T cells by flow cytometry and an increased mRNA level of the specific Th17 transcription factor retinoic acid-related orphan receptor γt in cocultures of LCs and responsive T cells in the presence of activated bEnd.3 cells. Experiments using the RNA interference technique to knockdown IL-6 in bEnd.3 cells confirmed that IL-6 produced by bEnd.3 cells stimulated by MDP is at least partially involved in Th17 polarization. Our data suggest that activated ECs are capable of influencing LC Ag processing and presentation to T cells and induce a Th17 polarization. These results are important for the understanding of Th17-related disorders of the skin such as psoriasis.

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Section: Discussionmentioning

confidence: 99%

Muramyl Dipeptide Induces Th17 Polarization through Activation of Endothelial Cells

Manni

Ding

Stohl

et al. 2011

The Journal of Immunology

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“…The following bacterial challenges have been used: Salmonella typhimurium [21], Salmonella enteritidis [57], Streptococcus pneumoniae [35], Pseudonomas aeruginosa, and Listeria monocytogenes [28,53]. Moreover, the activity of MDP was measured vis-a-vis two parasitic agents, Toxoplasma cruzi [37] and Toxoplasma 9ondii [43], and against a fungal infection, Candida albicans [53]. In certain immunocompromised hosts challenged by antibiotics sensitive or resistant pathogens, MDP was also shown to be capable of inducing a good level of resistance to infection [58,59].…”

Section: Enhancement Of Nonspecific Resistance To Bacterial Viral Omentioning

confidence: 99%

New approaches for control of infections using synthetic or semi-synthetic constructs containing MDP

Chedid

Audibert

1985

Springer Semin Immunopathol

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“…difficult to interpret; it could be argued that the protection observed following intradermal administration of killed M. leprae is mediated by nonspecific macrophage activation leading to enhanced resistance rather than the induction of a specific T-cell response. Indeed, mice undergoing local graft-versus-host disease (10) or animals treated with Corynebacterium parvum (5) show enhanced resistance to M. leprae infection, presumably due to the nonspecific effects of enhanced macrophage activation. However, in the former case the resistance was manifested as a slight retardation of growth of M. leprae, and in the experiments with C. parvum inoculation of the C. parvum directly into the footpad significantly limited growth in the inoculated footpad but not in the contralateral footpad.…”

mentioning

confidence: 99%

Vaccination of mice against Mycobacterium leprae infection

et al. 1989

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Intradermal immunization with killed Mycobacterium leprae renders mice immune to infection with viable M. leprae. This protection is long lasting and systemic in that immunization in the left flank results in protection in both the left and right footpads. Immunization with Mycobacterium vaccae was ineffective in protecting mice against M. leprae infection, while Mycobacterium bovis BCG provided partial protection. Mycobacterium habana TMC 5135 (now known as Mycobacterium simiae) was found to be as effective as M. leprae in protecting mice against footpad infection.

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Effects of treatment with muramyl dipeptide on resistance to Mycobacterium leprae and Mycobacterium marinum infection in mice

Cited by 7 publications

References 28 publications

Muramyl Dipeptide Induces Th17 Polarization through Activation of Endothelial Cells

Muramyl Dipeptide Induces Th17 Polarization through Activation of Endothelial Cells

New approaches for control of infections using synthetic or semi-synthetic constructs containing MDP

Vaccination of mice against Mycobacterium leprae infection

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