Mycolactone-mediated inhibition of tumor necrosis factor production by macrophages infected with Mycobacterium ulcerans has implications for the control of infection
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Mycolactone diffuses from Mycobacterium ulcerans-infected tissues and targets mononuclear cells in peripheral blood and lymphoid organsBacterial Toxins as Pathogen Weapons Against PhagocytesMycolactone-Dependent Depletion of Endothelial Cell Thrombomodulin Is Strongly Associated with Fibrin Deposition in Buruli Ulcer LesionsDetection of Mycolactone A/B in Mycobacterium ulcerans-Infected Human TissueAnalysis of the vaccine potential of plasmid DNA encoding nine mycolactone polyketide synthase domains in Mycobacterium ulcerans infected miceAccelerated detection of mycolactone production and response to antibiotic treatment in a mouse model of Mycobacterium ulcerans diseaseThe pathogenic mechanism of the Mycobacterium ulcerans virulence factor, mycolactone, depends on blockade of protein translocation into the ERGenetic Variation in Autophagy-Related Genes Influences the Risk and Phenotype of Buruli UlcerMycolactone gene expression is controlled by strong SigA-like promoters with utility in studies of Mycobacterium ulcerans and buruli ulcer.Improved protective efficacy of a species-specific DNA vaccine encoding mycolyl-transferase Ag85A from Mycobacterium ulcerans by homologous protein boostingAMP-activated protein kinase confers protection against TNF-{alpha}-induced cardiac cell death.Kinetics of mycolactone in human subcutaneous tissue during antibiotic therapy for Mycobacterium ulcerans diseaseContrasting persistence strategies in Salmonella and MycobacteriumProteomic analysis of the action of the Mycobacterium ulcerans toxin mycolactone: targeting host cells cytoskeleton and collagen.Clinical efficacy of combination of rifampin and streptomycin for treatment of Mycobacterium ulcerans disease.Cellular immunity confers transient protection in experimental Buruli ulcer following BCG or mycolactone-negative Mycobacterium ulcerans vaccination.Buruli ulcer.Macrophage cytokines: involvement in immunity and infectious diseasesPlatelets direct monocyte differentiation into epithelioid-like multinucleated giant foam cells with suppressive capacity upon mycobacterial stimulation.Mycobacterium ulcerans triggers T-cell immunity followed by local and regional but not systemic immunosuppression.Corticosteroid-induced immunosuppression ultimately does not compromise the efficacy of antibiotherapy in murine Mycobacterium ulcerans infection.Microbiological, histological, immunological, and toxin response to antibiotic treatment in the mouse model of Mycobacterium ulcerans diseasePhage therapy is effective against infection by Mycobacterium ulcerans in a murine footpad modelRecombinant BCG Expressing Mycobacterium ulcerans Ag85A Imparts Enhanced Protection against Experimental Buruli ulcer.Local and regional re-establishment of cellular immunity during curative antibiotherapy of murine Mycobacterium ulcerans infectionSpontaneous Healing of Mycobacterium ulcerans Lesions in the Guinea Pig ModelInterferon-γ Is a Crucial Activator of Early Host Immune Defense against Mycobacterium ulcerans Infection in Mice.Clinical Features of Spontaneous Partial Healing During Mycobacterium ulcerans Infection.Mycolactone activation of Wiskott-Aldrich syndrome proteins underpins Buruli ulcer formation.Mycolactones: immunosuppressive and cytotoxic polyketides produced by aquatic mycobacteria.Buruli ulcer: reductive evolution enhances pathogenicity of Mycobacterium ulcerans.History, biology and chemistry of Mycobacterium ulcerans infections (Buruli ulcer disease).Pleiotropic molecular effects of the Mycobacterium ulcerans virulence factor mycolactone underlying the cell death and immunosuppression seen in Buruli ulcer.Mycolactone reveals the substrate-driven complexity of Sec61-dependent transmembrane protein biogenesis.Investigation of wild-type and mycolactone-negative mutant Mycobacterium ulcerans on skeletal muscle: IGF-1 protects against mycolactone-induced muscle catabolism.Independent loss of immunogenic proteins in Mycobacterium ulcerans suggests immune evasion.FVB/N Mice Spontaneously Heal Ulcerative Lesions Induced by Mycobacterium ulcerans and Switch M. ulcerans into a Low Mycolactone Producer.Infiltrating leukocytes surround early Buruli ulcer lesions, but are unable to reach the mycolactone producing mycobacteria.Mechanistic insights into the inhibition of Sec61-dependent co- and post-translational translocation by mycolactone.[Buruli ulcer: a dynamic transversal research model performed through the international network of Pasteur Institutes].
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P2860
Mycolactone-mediated inhibition of tumor necrosis factor production by macrophages infected with Mycobacterium ulcerans has implications for the control of infection
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
2007年论文
@zh
2007年论文
@zh-cn
name
Mycolactone-mediated inhibitio ...... s for the control of infection
@ast
Mycolactone-mediated inhibitio ...... s for the control of infection
@en
type
label
Mycolactone-mediated inhibitio ...... s for the control of infection
@ast
Mycolactone-mediated inhibitio ...... s for the control of infection
@en
prefLabel
Mycolactone-mediated inhibitio ...... s for the control of infection
@ast
Mycolactone-mediated inhibitio ...... s for the control of infection
@en
P2860
P50
P356
P1476
Mycolactone-mediated inhibitio ...... s for the control of infection
@en
P2093
Pamela L C Small
Sarojini Adusumilli
P2860
P304
P356
10.1128/IAI.00290-07
P407
P577
2007-05-21T00:00:00Z