Human phagocyte oxidative burst activation by BCG, M. leprae, and atypical mycobacteria: Defective activation by M. leprae is not reversed by interferon γ

Launois, Pascal; Maillère, Bernard; Dièye, Alioune; Sarthou, Jean-Louis; Bach, M A

doi:10.1016/0008-8749(89)90120-2

Cited by 9 publications

(4 citation statements)

References 27 publications

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“…However, M. leprae suspensions do demonstrate superoxide dismutase (Wheeler & Gregory, 1980;Thangaraj et al, 1990) and express both sodC and sodA (Williams et al, 2004). Additional indirect evidence supports a hypothesis that the ability of M. leprae to suppress the oxidative burst is a virulence factor and stems from studies at the cellular level where M. leprae or its constituents were shown to suppress host ROI production (Holzer et al, 1986;Sibley & Krahenbuhl, 1988a, b;Launois et al, 1989;Schlesinger & Horwitz, 1991) or scavenge ROI (Neill & Klebanoff, 1988;Chan et al, 1989;Vachula et al, 1989;Moura et al, 1997).…”

Section: Introductionmentioning

confidence: 85%

Emergence of an effective adaptive cell mediated immune response toMycobacterium lepraeis not impaired in reactive oxygen intermediate-deficient mice

Hagge

Marks

Ray

et al. 2007

FEMS Immunology &Amp; Medical Microbiology

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Cytokine-activated macrophages (MF) employ reactive oxygen intermediates (ROI) and reactive nitrogen intermediates (RNI) to combat pathogens. The requirement for ROI for an effective host response to experimental leprosy using mice which have a disruption in the 91-kD subunit of the NAPDH oxidase cytochrome b (phox91 CD62Lhi cells and was, therefore, not representative of the infection site. TH1 cytokines, chemokines and inducible nitric oxide synthase were comparably expressed in the FP of both strains. When infected in vitro, normal MF from B6 and phox91 À/À mice supported bacterial viability, whereas IFNg-activated MF killed M. leprae in a RNI-dependent manner, emphasizing that ROI was dispensable. These data show that phox91 À/À mice generate a strong adaptive immune response and control long-term infection with M. leprae.

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Section: Introductionmentioning

confidence: 85%

Emergence of an effective adaptive cell mediated immune response toMycobacterium lepraeis not impaired in reactive oxygen intermediate-deficient mice

Hagge

Marks

Ray

et al. 2007

FEMS Immunology &Amp; Medical Microbiology

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“…As TNF-c~ might enhance the respiratory burst from mononuclear cells we investigated the capacity of r-TNF-a to induce a CL response from mononuclear cells in the presence of M. leprae, r-TNF-a could increase the M. bouis BCG but not the M. lepraeinduced CL response. M. leprae has been previously described to fail to produce oxygen-free radicals [16,17]. Phenolic glycolipid-1 unique to M. leprae [26] and lipoarabinomannan [27] acting as a scavenger of reactive oxygen species, could explain in part this phenomenon.…”

Section: Discussionmentioning

confidence: 99%

“…1). Thus, further studies were performed with a constant concen-93 tration of 100 IU/ml of r-TNF-a and a preincubation of 2 h. As previously described [16,17], M. leprae failed to trigger any response in mononuclear cells from healthy subjects. Conversely, M. boris BCG elicited a strong response ( Fig.…”

Section: Effects Of R-tnf-a On Bcg and M Leprae-induced Chemiluminesmentioning

confidence: 99%

TNF-α failed to reverse the M. leprae-induced defective chemiluminescence response of human mononuclear cells

Launois¹

1992

FEMS Microbiology Letters

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The effect of phagocyte activation by TNF‐α on the ability to trigger a chemiluminescence (CL) response, associated with the release of oxidizing species was evaluated in healthy human mononuclear cells in the presence of Mycobacterium leprae. Recombinant TNF‐α (r‐TNF‐α) increased the CL response of unstimulated M. bovis BCG‐ and PMA‐stimulated cells but did not reverse the M. leprae defective activation of the human phagocyte oxidative burst. M. leprae was less well phagocytosed than M. bovis BCG but phagocytosis of mycobacteria was not altered by addition of r‐TNF‐α. The failure of activation of oxygen‐free radical production might have some relevance to the pathogenesis of leprosy.

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“…In-vitro-Experimente unserer Gruppe und anderer zeigten, dass autoklavierte mykobakterielle Präparationen eine geringere Aktivierung von Granulozyten hervorriefen als viable Präparationen [15,32,33]. In unseren Tierversuchen jedoch zeigte sich kein signifikanter therapeutischer Effekt von aBCG auf das Überleben und das Blasengewicht von Mäusen im Vergleich zu viablem BCG.…”

Section: Diskussionunclassified

Optimierung des orthotopen murinen Harnblasenkarzinom-Modells und Einsatz zur Untersuchung der intravesikalen Bacillus Calmette-Guérin Immuntherapie

Jurczok¹,

Günther²,

Durek³

et al. 2000

Aktuel Urol

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Human phagocyte oxidative burst activation by BCG, M. leprae, and atypical mycobacteria: Defective activation by M. leprae is not reversed by interferon γ

Cited by 9 publications

References 27 publications

Emergence of an effective adaptive cell mediated immune response toMycobacterium lepraeis not impaired in reactive oxygen intermediate-deficient mice

Emergence of an effective adaptive cell mediated immune response toMycobacterium lepraeis not impaired in reactive oxygen intermediate-deficient mice

TNF-α failed to reverse the M. leprae-induced defective chemiluminescence response of human mononuclear cells

Optimierung des orthotopen murinen Harnblasenkarzinom-Modells und Einsatz zur Untersuchung der intravesikalen Bacillus Calmette-Guérin Immuntherapie

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