Antagonization of TNF attenuates systemic hemodynamic manifestations of envenomation in a rat model of Vipera aspis snakebite

Szold, Oded; Ben‐Abraham, Ron; Weinbroum, Avi A.; Englender, Talma; Ovadia, Dror; Sorkine, M.; Bon, Cassian; Flaison, Ron; Sorkine, Patrick

doi:10.1007/s001340100875

Cited by 14 publications

(4 citation statements)

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“…Venom-treated cells also produced very high NO levels, as one would expect from the presence of cytokines able to induce iNOS. Venom from the asp, Vipera aspis, increases serum TNF levels in rats (390); either anti-TNF antibody or soluble TNF receptor (p55), when injected at the same time as the venom, prevented certain harmful changes (389). Further study by this group has demonstrated that TNF is the cause of deleterious cardiac effects induced by this venom, in that anti-TNF antibody prevented these changes (388).…”

Section: Pathology Caused By Snake Venommentioning

confidence: 99%

Pathogenesis of Malaria and Clinically Similar Conditions

et al. 2004

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There is now wide acceptance of the concept that the similarity between many acute infectious diseases, be they viral, bacterial, or parasitic in origin, is caused by the overproduction of inflammatory cytokines initiated when the organism interacts with the innate immune system. This is also true of certain noninfectious states, such as the tissue injury syndromes. This review discusses the historical origins of these ideas, which began with tumor necrosis factor (TNF) and spread from their origins in malaria research to other fields. As well the more established proinflammatory mediators, such as TNF, interleukin-1, and lymphotoxin, the roles of nitric oxide and carbon monoxide, which are chiefly inhibitory, are discussed. The established and potential roles of two more recently recognized contributors, overactivity of the enzyme poly(ADP-ribose) polymerase 1 (PARP-1) and the escape of high-mobility-group box 1 (HMGB1) protein from its normal location into the circulation, are also put in context. The pathogenesis of the disease caused by falciparum malaria is then considered in the light of what has been learned about the roles of these mediators in these other diseases, as well as in malaria itself

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Section: Pathology Caused By Snake Venommentioning

confidence: 99%

Pathogenesis of Malaria and Clinically Similar Conditions

et al. 2004

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“…Another rat study in 2000 reported by Petricevich et al 15 showed that B. asper and Bothrops jararaca venom that was given intraperitoneally increased TNFα and IL-6 levels. Szold et al 16 reported that rats given Vipera apsis venom had increased systemic TNFα and local tissue damage. This study was divided into four groups; group 1 received only venom, group 2 was injected with venom and anti-TNFα antibody, group 3 was injected with venom and soluble TNFα receptor and group 4 was a control group.…”

Section: Discussionmentioning

confidence: 99%

Serum IL-6, TNF levels in snakebite cases occurring in Southern Turkey

Açıkalın

Gökel

2010

Emergency Medicine Journal

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“…Reported to be safe and efficacious in a small clinical trial [97] Autoimmune encephalomyelitis Ameliorated experimental autoimmune encephalomyelitis [98][99][100]; however, failed to show benefits in a Phase II study with lenercept [79] Experimental painful neuropathy Reduced thermal hyperalgesia and allodynia in a mouse model after either topical or systemic administration [101] Spondyloarthropathies Remarkably effective in improving the clinical manifestations of resistant spondyloarthropathy [102,103]; achieved rapid remission in refractory ankylosing spondylitis [103,104] Corneal graft rejection Gene transfer of a receptor increased graft survival [105] Experimental glomerular nephritis Reduced glomerular damage along with decreased infiltration of neutrophils and monocytes in an accelerated rat model [106] Vipera aspis snakebite Blunted haemodynamic changes in a rat model of envenomation [107] Fever and sleepiness Treated hereditary periodic fever and warming-induced sleep responses in rabbits [108,109] LPS: Lipopolysaccharide; sTNFR: Soluble TNF receptor.…”

Section: Diabetesmentioning

confidence: 99%

Soluble cytokine receptors in biological therapy

Fernández-Botrán

Crespo

Sun

2002

Expert Opinion on Biological Therapy

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Due to their fundamental involvement in the pathogenesis of many diseases, cytokines constitute key targets for biotherapeutic approaches. The discovery that soluble forms of cytokine receptors are involved in the endogenous regulation of cytokine activity has prompted substantial interest in their potential application as immunotherapeutic agents. As such, soluble cytokine receptors have many advantages, including specificity, low immunogenicity and high affinity. Potential disadvantages, such as low avidity and short in vivo half-lifes, have been addressed by the use of genetically-designed receptors, hybrid proteins or chemical modifications. The ability of many soluble cytokine receptors to inhibit the binding and biological activity of their ligands makes them very specific cytokine antagonists. Several pharmaceutical companies have generated a number of therapeutic agents based on soluble cytokine receptors and many of them are undergoing clinical trials. The most advanced in terms of clinical development is etanercept (Enbrel, Immunex), a fusion protein between soluble TNF receptor Type II and the Fc region of human IgG1. This TNF-alpha; antagonist was the first soluble cytokine receptor to receive approval for use in humans. In general, most agents based on soluble cytokine receptors have been safe, well-tolerated and have shown only minor side effects in the majority of patients. Soluble cytokine receptors constitute a new generation of therapeutic agents with tremendous potential for applications in a wide variety of human diseases. Two current areas of research are the identification of their most promising applications and characterisation of their long-term effects.

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Antagonization of TNF attenuates systemic hemodynamic manifestations of envenomation in a rat model of Vipera aspis snakebite

Abstract: The hemodynamic consequences of intramuscular injection of V. aspis venom can be blunted in a rat by systemic antagonization of TNF activity prior to venom injection. The poisonous hemodynamic effects of the V. aspis venom might be caused by systemic release of TNF.

Cited by 14 publications

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Pathogenesis of Malaria and Clinically Similar Conditions

Pathogenesis of Malaria and Clinically Similar Conditions

Serum IL-6, TNF levels in snakebite cases occurring in Southern Turkey

Soluble cytokine receptors in biological therapy

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