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           Search results for: Rat monoclonal anti mouse Interleukin 6 Anti-Mouse antibodies   

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#10381487   1999/08/06 Save this To Up

Anti-inflammatory effects of systemic anti-tumour necrosis factor alpha treatment in human/murine SCID arthritis.

To evaluate in vivo the contribution of tumour necrosis factor alpha (TNFalpha) to the chimeric transfer model of human rheumatoid arthritis synovial membrane into SCID mice (hu/mu SCID arthritis), systemic anti-TNFalpha treatment was performed and the clinical, serological, and histopathological effects of this treatment assessed.

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Mouse Anti-Human Interleu RABBIT ANTI HUMAN SDF-1 A Mouse Anti-Human Inhibin Mouse Anti-Human Integrin Rabbit Anti-Human Inhibin Rabbit Anti-Human NFkB In Goat Anti-Human Alpha2-an Goat Anti-Human Catenin a Goat Anti-Human CBX5 HP1- Goat Anti-Human Complemen Goat Anti-Human Factor XI Goat Anti-Human Fibroblas

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#7634801   1995/09/14 Save this To Up

Contribution of tumor necrosis factor-alpha to pulmonary cytokine expression and lung injury after hemorrhage and resuscitation.

To examine the role of tumor necrosis factor-alpha (TNF-alpha) in producing acute inflammatory lung injury after hemorrhage and resuscitation.

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ELISA Kit for Tumor Necr Human Tumor Necrosis Fact TNFRSF1B - Goat polyclona Mouse Tumor Necrosis Fact Rat Tumor Necrosis Factor ELISA Kit for Tumor Necro Mouse Tumor Necrosis Fact Human Tumor Necrosis Fact Tumor necrosis factor (TN Human Tumor Necrosis Fact RANK Ligand Soluble, Huma ELISA p55,p60,Pig,Sus scr

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#8336076   1993/08/25 Save this To Up

Lipopolysaccharide-induced cytokine production and mortality in mice treated with Corynebacterium parvum.

Tumor necrosis factor alpha (TNF-alpha) has been shown to be an important mediator of the lethal effects of endotoxin in several experimental models of septic shock. However, studies with a recombinant human interleukin-1 (IL-1) receptor antagonist protein (IL-1ra) suggest a role for IL-1 as a mediator of septic shock as well. In the present study, we show that mice treated in vivo with Corynebacterium parvum are primed for the production of interferon-gamma (IFN-gamma) and exhibit an enhanced capacity to produce serum IL-1 alpha, TNF-alpha, and IL-6 when challenged intravenously with lipopolysaccharide (LPS). The majority of C. parvum-treated mice die within 24 h of an LPS challenge. Pretreatment with a rat antimouse TNF-alpha monoclonal antibody (mAb) protected 90% of the animals against the lethal endotoxin challenge, while an anti-IFN-gamma mAb gave approximately 75% protection. The anti-IFN-gamma mAb also caused a reduction in LPS-induced serum TNF-alpha and IL-1 alpha. Anti-IL-1 alpha, anti-IL-1 beta, and anti-IL-6 neutralizing mAb did not protect against lethality when administered to mice prior to the LPS challenge. These results indicate that TNF-alpha and IFN-gamma are major mediators of endotoxin shock in C. parvum-treated mice. The results further suggest that the IFN-gamma produced by C. parvum-primed mice in response to an LPS challenge serves as a stimulus for enhanced production of TNF-alpha and IL-1 alpha. These findings are consistent with an increasing body of evidence suggesting a major role for IFN-gamma in lethal endotoxemia.

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Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Human Epstein-Barr Virus Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Macrophage Colony Stimula Macrophage Colony Stimula Mouse Epstein-Barr Virus

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