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Effects of recombinant dimeric TNF receptor on human inflammatory responses following intravenous endotoxin administration

Suffredini, AF ; Reda, D ; Banks, SM ; Tropea, M ; Agosti, JM ; Miller, R

The Journal of immunology (1950), 1995-11, Vol.155 (10), p.5038-5045 [Periódico revisado por pares]

United States: Am Assoc Immnol

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  • Título:
    Effects of recombinant dimeric TNF receptor on human inflammatory responses following intravenous endotoxin administration
  • Autor: Suffredini, AF ; Reda, D ; Banks, SM ; Tropea, M ; Agosti, JM ; Miller, R
  • Assuntos: Animals ; Endotoxins - adverse effects ; Etanercept ; Female ; Humans ; Immunoglobulin G - immunology ; Immunotherapy ; Inflammation - etiology ; Inflammation - immunology ; Inflammation - therapy ; Injections, Intravenous ; Male ; Mice ; Receptors, Tumor Necrosis Factor - immunology ; Recombinant Proteins - immunology
  • É parte de: The Journal of immunology (1950), 1995-11, Vol.155 (10), p.5038-5045
  • Notas: ObjectType-Article-2
    SourceType-Scholarly Journals-1
    ObjectType-Feature-1
    content type line 23
    ObjectType-News-3
  • Descrição: Effects of dimeric TNF receptor (p80) Fc (TNFR:Fc) on acute phase responses were evaluated in 18 volunteers given endotoxin (4 ng/kg i.v.). Subjects were randomized to receive either placebo (n = 6), low dose TNFR:Fc (10 mg/m2 i.v., n = 6), or high dose TNFR:Fc (60 mg/m2 i.v., n = 6). TNFR:Fc blocked plasma TNF bioactivity (p = 0.001) and increased, in a dose-ordered fashion, TNF immunoactivity (p < 0.001). TNFR:Fc decreased secondary cytokine levels including IL-1 beta (p = 0.007), IL-8 (p < 0.001), IL-1 receptor antagonist (p < 0.001), granulocyte-CSF (p = 0.03), and growth regulated peptide-alpha (p = 0.001) but not macrophage inflammatory protein-1 alpha or IL-10. Low dose, but not high dose, TNFR:Fc blunted or delayed the release of epinephrine and cortisol (p < or = 0.026). Despite the absence of plasma TNF bioactivity, high dose TNFR:Fc was less immunosuppressive than low dose TNFR:Fc as measured by cytokine and stress hormone responses. Endotoxin-related symptoms were not altered by TNFR:Fc and the febrile response was delayed but not diminished (p = 0.004). Increases in cardiac index (72 +/- 19%) and heart rate (60 +/- 10%) and decreases in systemic vascular resistance index (47 +/- 7%) were unaltered by TNFR:Fc. These data suggest that the inflammatory response to endotoxin can escape from high levels of circulating TNF-blocking activity and redundant pathways, independent of circulating TNF, can sustain inflammation and clinical responses caused by acute endotoxemia.
  • Editor: United States: Am Assoc Immnol
  • Idioma: Inglês
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