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MeSH Review

Shock, Septic

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Disease relevance of Shock, Septic


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Chemical compound and disease context of Shock, Septic


Biological context of Shock, Septic

  • Tumor necrosis factor (TNF, TNFalpha) is implicated in various pathophysiological processes and can be either protective, as in host defense, or deleterious, as in autoimmunity or toxic shock [18].
  • Sequences in both class II major histocompatibility complex alpha and beta chains contribute to the binding of the superantigen toxic shock syndrome toxin 1 [19].
  • To characterize these interactions at the molecular level, random point mutations were generated in the gene encoding toxic shock syndrome toxin 1, a bacterial superantigen associated with toxic shock syndrome [20].
  • Endotoxin, a bacterial lipopolysaccharide (LPS), causes fatal septic shock via Toll-like receptor (TLR)4 on effector cells of innate immunity like macrophages, where it activates nuclear factor kappaB (NF-kappaB) and mitogen-activated protein (MAP) kinases to induce proinflammatory cytokines such as tumor necrosis factor (TNF)-alpha [21].
  • This study evaluates in dogs the effect of the C1-esterase inhibitor (C1-INH), a main inhibitor of the blood coagulation contact system, on the cardiovascular and respiratory dysfunction associated with endotoxic shock [22].
  • Proinflammatory cytokines have been linked to depression of myocardial contractility in vivo in patients with acute septic shock and in vitro models employing isolated myocytes exposed to serum from such patients. The key pathways involved in mediating this septic organ dysfunction (cell adhesion molecule expression, inducible nitric-oxide synthase induction, and apoptosis) are known to be regulated by transcription factors STAT1, IRF1, and NF-kappaB. Utilizing a model that mimics human disease, it was demonstrated that activation of the transcription factors STAT1, IRF1, and NF-kappaB occurs in human fetal myocytes exposed to human septic serum. Both reporter and electrophoretic mobility shift assays demonstrated a 5-19-fold increase in activation of transcription factors STAT1, IRF1, and NF-kappaB in response to incubation with human septic serum. The addition of human septic serum to human fetal myocytes induced apoptosis in human fetal myocytes and activation of the mitogen-activated protein kinase c-Jun NH -terminal kinase and caspase 1 as measured by Western blot. These data suggest that transcription factor activation and early myocyte apoptosis play a mechanistic role in septic myocardial depression and sepsis-induced organ dysfunction. [23]

Anatomical context of Shock, Septic


Gene context of Shock, Septic


Analytical, diagnostic and therapeutic context of Shock, Septic



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  19. Sequences in both class II major histocompatibility complex alpha and beta chains contribute to the binding of the superantigen toxic shock syndrome toxin 1. Braunstein, N.S., Weber, D.A., Wang, X.C., Long, E.O., Karp, D. J. Exp. Med. (1992) [Pubmed]
  20. Identification of class II major histocompatibility complex and T cell receptor binding sites in the superantigen toxic shock syndrome toxin 1. Hurley, J.M., Shimonkevitz, R., Hanagan, A., Enney, K., Boen, E., Malmstrom, S., Kotzin, B.L., Matsumura, M. J. Exp. Med. (1995) [Pubmed]
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  25. The macrophage scavenger receptor type A is expressed by activated macrophages and protects the host against lethal endotoxic shock. Haworth, R., Platt, N., Keshav, S., Hughes, D., Darley, E., Suzuki, H., Kurihara, Y., Kodama, T., Gordon, S. J. Exp. Med. (1997) [Pubmed]
  26. The CD4 molecule is not always required for the T cell response to bacterial enterotoxins. Sékaly, R.P., Croteau, G., Bowman, M., Scholl, P., Burakoff, S., Geha, R.S. J. Exp. Med. (1991) [Pubmed]
  27. Endothelial cells require STAT3 for protection against endotoxin-induced inflammation. Kano, A., Wolfgang, M.J., Gao, Q., Jacoby, J., Chai, G.X., Hansen, W., Iwamoto, Y., Pober, J.S., Flavell, R.A., Fu, X.Y. J. Exp. Med. (2003) [Pubmed]
  28. Bacterial lipopolysaccharides prime human neutrophils for enhanced production of leukotriene B4. Doerfler, M.E., Danner, R.L., Shelhamer, J.H., Parrillo, J.E. J. Clin. Invest. (1989) [Pubmed]
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