Induction of Endothelial Cell/Macrophage Procoagulant Activity: Synergistic Stimulation by Gamma Interferon and Granulocyte-Macrophage Colony Stimulating Factor

Zuckerman, S; Ym, Suprenant

doi:10.1055/s-0038-1646555

Cited by 35 publications

(14 citation statements)

References 6 publications

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“…These data suggest that GM-CSF, but not G-CSF, induces an activation of coagulation. These data are in keeping with experimental data previously reported [5,23,27]. This activation of the coagulation system is presumably responsible for the increased AT consumption in our GM-CSF treated patients.…”

Section: Discussionsupporting

confidence: 94%

Growth factors and hemostasis: differential effects of GM-CSF and G-CSF on coagulation activation – laboratory and clinical evidence

et al. 2001

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Section: Discussionsupporting

confidence: 94%

Growth factors and hemostasis: differential effects of GM-CSF and G-CSF on coagulation activation – laboratory and clinical evidence

et al. 2001

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“…N O in SEB-induced shock not only downregulates the production of inflammatory cytokines as shown in this paper but might also reduce their pathogenic effects. As a matter of fact, the vasoactive properties of N O as well as its ability to inhibit platelet aggregation and adhesion could be important in counteracting the prothrombotic properties of TNF and IFN-3, (24,25). Indeed, we observed lesions of coagulative necrosis in the liver of mice coinjected with SEB and induced by SEB in L-NAME-treated mice.…”

Section: Inhibition Of No Synthesis Enhances Ifn-9 and Tnf Synthesismentioning

confidence: 73%

The protective role of endogenously synthesized nitric oxide in staphylococcal enterotoxin B-induced shock in mice.

Florquin

Amraoui

Dubois

et al. 1994

The Journal of Experimental Medicine

206

139

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SummaryNitric oxide (NO) synthesis during experimental endotoxemia has been shown to have both deleterious and beneficial effects. In the present study, we analyzed the in vivo production and the regulatory role of NO in the shock syndrome induced by staphylococcal enterotoxin B (SEB) in mice. First, we found that intraperitoneal administration of 100/xg SEB in BALB/c mice induced a massive synthesis of NO as indicated by high serum levels of nitrite (NO2-) and nitrate (NO3-) peaking 16 h after SEB injection. The inhibition of NO2-and NO3-release in mice injected with anti-tumor necrosis factor (TNF) and/or anti-interferon "y (IFN-~/) monoclonal antibody (mAb) before SEB challenge revealed that both cytokines were involved in SEB-induced NO overproduction. In vitro experiments indicated that NO synthase (NOS) inhibition by N-nitro-t-arginine methyl ester (L-NAME) enhanced IFN-~/and TNF production by splenocytes in response to SEB. A similar effect was observed in vivo as treatment of mice with L-NAME resulted in increased IFN-3' and TNF serum levels 24 h after SEB challenge, together with persistent expression of corresponding cytokine mKNA in spleen. The prolonged production of inflammatory cytokines in mice receiving L-NAME and SEB was associated with a 95% mortality rate within 96 h, whereas all mice survived injections of SEB or t-NAME alone. Both TNF and IFN-3' were responsible for the lethality induced by SEB in L-NAME-treated mice as shown by the protection provided by simultaneous administration of anti-IFN-~/and anti-TNF mAbs. We conclude the SEB induces NO synthesis in vivo and that endogenous NO has protective effects in this model of T cell-dependent shock by downregulating IFN-3' and TNF production.

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“…Herein, we reported that anti-CD3 MoAb induces a systemic release of NO metabolites and that the priming for IFN-and TNF-production in the course of T. cruzi infection is responsible, at least in part, for this NO overproduction. Although NO was involved in the haemodynamic changes occurring during septic shock [28], the vasoactive properties of NO as well as its ability to inhibit platelet aggregation and adhesion might protect vital organs from the prothrombotic properties of IFN-and TNF- [37,38]. Indeed, inhibition of the constitutive and inducible forms of NOS by agents such as L-NAME was previously shown to increase the toxicity of bacterial toxins [26,29].…”

Section: Discussionmentioning

confidence: 99%

Administration of anti-CD3 monoclonal antibody during experimental Chagas’ disease induces CD8+ cell-dependent lethal shock

Jacobs

Dubois

Carlier

et al. 1996

Clinical and Experimental Immunology

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SUMMARYThe injection of the 145-2C11 anti-CD3 MoAb in mice induces a polyclonal T cell activation resulting in the release of several cytokines, including interferon-gamma (IFN-) and tumour necrosis factoralpha (TNF-). As these cytokines are known to be involved in the host defence against Trypanosoma cruzi, we measured serum levels of IFN-and TNF-after injection of the 145-2C11 MoAb in the course of experimental murine Chagas' disease. Compared with control mice, T. cruzi-infected BALB/c mice were found to be primed to secrete very high levels of IFN-and TNF-from the second and the first week of infection, respectively, up to the chronic phase. In vivo cell depletion experiments indicated that CD8 T cells were responsible for these dramatic hyperproductions of IFN-and TNF-. While all control mice survived anti-CD3 MoAb injection, a high lethality rate was observed in T. cruzi-infected mice within 24 h after anti-CD3 MoAb challenge. Pretreatment with neutralizing anti-IFN-MoAb or depletion of CD8 T cell population dramatically decreased the mortality induced by anti-CD3 MoAb in T. cruzi-infected mice. Finally, we showed that anti-CD3 MoAb injection in T. cruzi-infected mice was followed by a massive release of nitric oxide (NO) metabolites, which was partially reduced by IFN-or TNF-neutralization. The administration of the NO synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME) before anti-CD3 MoAb challenge did not prevent and even enhanced lethality in T. cruzi-infected mice, suggesting that NO overproduction and lethal shock are not causally related. We conclude that injection of anti-CD3 MoAb in the course of experimental Chagas' disease induces a CD8 cell-dependent shock mediated by IFN-and TNF-.

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Induction of Endothelial Cell/Macrophage Procoagulant Activity: Synergistic Stimulation by Gamma Interferon and Granulocyte-Macrophage Colony Stimulating Factor

Cited by 35 publications

References 6 publications

Growth factors and hemostasis: differential effects of GM-CSF and G-CSF on coagulation activation – laboratory and clinical evidence

Growth factors and hemostasis: differential effects of GM-CSF and G-CSF on coagulation activation – laboratory and clinical evidence

The protective role of endogenously synthesized nitric oxide in staphylococcal enterotoxin B-induced shock in mice.

Administration of anti-CD3 monoclonal antibody during experimental Chagas’ disease induces CD8+ cell-dependent lethal shock

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