The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Shock, Septic

 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

Disease relevance of Shock, Septic

 

Psychiatry related information on Shock, Septic

 

High impact information on Shock, Septic

 

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

 

References

  1. A controlled clinical trial of high-dose methylprednisolone in the treatment of severe sepsis and septic shock. Bone, R.C., Fisher, C.J., Clemmer, T.P., Slotman, G.J., Metz, C.A., Balk, R.A. N. Engl. J. Med. (1987) [Pubmed]
  2. A novel form of TNF/cachectin is a cell surface cytotoxic transmembrane protein: ramifications for the complex physiology of TNF. Kriegler, M., Perez, C., DeFay, K., Albert, I., Lu, S.D. Cell (1988) [Pubmed]
  3. Cloning of a new cytokine that induces IFN-gamma production by T cells. Okamura, H., Tsutsi, H., Komatsu, T., Yutsudo, M., Hakura, A., Tanimoto, T., Torigoe, K., Okura, T., Nukada, Y., Hattori, K. Nature (1995) [Pubmed]
  4. Essential role of MD-2 in LPS responsiveness and TLR4 distribution. Nagai, Y., Akashi, S., Nagafuku, M., Ogata, M., Iwakura, Y., Akira, S., Kitamura, T., Kosugi, A., Kimoto, M., Miyake, K. Nat. Immunol. (2002) [Pubmed]
  5. Staphylococcus aureus isolates from patients with nonmenstrual toxic shock syndrome. Evidence for additional toxins. Garbe, P.L., Arko, R.J., Reingold, A.L., Graves, L.M., Hayes, P.S., Hightower, A.W., Chandler, F.W., Broome, C.V. JAMA (1985) [Pubmed]
  6. The effect of stress doses of hydrocortisone during septic shock on posttraumatic stress disorder in survivors. Schelling, G., Briegel, J., Roozendaal, B., Stoll, C., Rothenhäusler, H.B., Kapfhammer, H.P. Biol. Psychiatry (2001) [Pubmed]
  7. Modulatory role of the epinergic system in the neuroendocrine-immune system function. Giovambattista, A., Chisari, A.N., Gaillard, R.C., Spinedi, E. Neuroimmunomodulation (2000) [Pubmed]
  8. Specific ablation of Stat3beta distorts the pattern of Stat3-responsive gene expression and impairs recovery from endotoxic shock. Yoo, J.Y., Huso, D.L., Nathans, D., Desiderio, S. Cell (2002) [Pubmed]
  9. Murine caspase-11, an ICE-interacting protease, is essential for the activation of ICE. Wang, S., Miura, M., Jung, Y.K., Zhu, H., Li, E., Yuan, J. Cell (1998) [Pubmed]
  10. Treatment of septic shock with the tumor necrosis factor receptor:Fc fusion protein. The Soluble TNF Receptor Sepsis Study Group. Fisher, C.J., Agosti, J.M., Opal, S.M., Lowry, S.F., Balk, R.A., Sadoff, J.C., Abraham, E., Schein, R.M., Benjamin, E. N. Engl. J. Med. (1996) [Pubmed]
  11. Tumor necrosis factor receptor: Fc fusion protein in septic shock. Whiteley, M.S. N. Engl. J. Med. (1996) [Pubmed]
  12. Mice deficient in IL-1 beta-converting enzyme are defective in production of mature IL-1 beta and resistant to endotoxic shock. Li, P., Allen, H., Banerjee, S., Franklin, S., Herzog, L., Johnston, C., McDowell, J., Paskind, M., Rodman, L., Salfeld, J. Cell (1995) [Pubmed]
  13. Prostaglandins, leukotrienes, and platelet-activating factor in shock. Feuerstein, G., Hallenbeck, J.M. Annu. Rev. Pharmacol. Toxicol. (1987) [Pubmed]
  14. Prognostic value of cortisol response in septic shock. Marik, P., Zaloga, G. JAMA (2000) [Pubmed]
  15. Nitric oxide and septic shock. Cobb, J.P., Danner, R.L. JAMA (1996) [Pubmed]
  16. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. Annane, D., Sébille, V., Charpentier, C., Bollaert, P.E., François, B., Korach, J.M., Capellier, G., Cohen, Y., Azoulay, E., Troché, G., Chaumet-Riffaut, P., Bellissant, E. JAMA (2002) [Pubmed]
  17. Mice deficient in IL-1beta manifest impaired contact hypersensitivity to trinitrochlorobenzone. Shornick, L.P., De Togni, P., Mariathasan, S., Goellner, J., Strauss-Schoenberger, J., Karr, R.W., Ferguson, T.A., Chaplin, D.D. J. Exp. Med. (1996) [Pubmed]
  18. Distinct and nonredundant in vivo functions of TNF produced by t cells and macrophages/neutrophils: protective and deleterious effects. Grivennikov, S.I., Tumanov, A.V., Liepinsh, D.J., Kruglov, A.A., Marakusha, B.I., Shakhov, A.N., Murakami, T., Drutskaya, L.N., Förster, I., Clausen, B.E., Tessarollo, L., Ryffel, B., Kuprash, D.V., Nedospasov, S.A. Immunity (2005) [Pubmed]
  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]
  21. Dok-1 and Dok-2 are negative regulators of lipopolysaccharide-induced signaling. Shinohara, H., Inoue, A., Toyama-Sorimachi, N., Nagai, Y., Yasuda, T., Suzuki, H., Horai, R., Iwakura, Y., Yamamoto, T., Karasuyama, H., Miyake, K., Yamanashi, Y. J. Exp. Med. (2005) [Pubmed]
  22. Endotoxin-induced pulmonary dysfunction is prevented by C1-esterase inhibitor. Guerrero, R., Velasco, F., Rodriguez, M., Lopez, A., Rojas, R., Alvarez, M.A., Villalba, R., Rubio, V., Torres, A., del Castillo, D. J. Clin. Invest. (1993) [Pubmed]
  23. Human serum from patients with septic shock activates transcription factors STAT1, IRF1, and NF-kappaB and induces apoptosis in human cardiac myocytes. Kumar, A., Kumar, A., Michael, P., Brabant, D., Parissenti, A.M., Ramana, C.V., Xu, X., Parrillo, J.E. J. Biol. Chem. (2005) [Pubmed]
  24. Structures of free and inhibited human secretory phospholipase A2 from inflammatory exudate. Scott, D.L., White, S.P., Browning, J.L., Rosa, J.J., Gelb, M.H., Sigler, P.B. Science (1991) [Pubmed]
  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]
  29. Heme oxygenase-1 mediates the anti-inflammatory effect of interleukin-10 in mice. Lee, T.S., Chau, L.Y. Nat. Med. (2002) [Pubmed]
  30. Human CD14 mediates recognition and phagocytosis of apoptotic cells. Devitt, A., Moffatt, O.D., Raykundalia, C., Capra, J.D., Simmons, D.L., Gregory, C.D. Nature (1998) [Pubmed]
  31. Involvement of receptor-interacting protein 2 in innate and adaptive immune responses. Chin, A.I., Dempsey, P.W., Bruhn, K., Miller, J.F., Xu, Y., Cheng, G. Nature (2002) [Pubmed]
  32. ROS-dependent activation of the TRAF6-ASK1-p38 pathway is selectively required for TLR4-mediated innate immunity. Matsuzawa, A., Saegusa, K., Noguchi, T., Sadamitsu, C., Nishitoh, H., Nagai, S., Koyasu, S., Matsumoto, K., Takeda, K., Ichijo, H. Nat. Immunol. (2005) [Pubmed]
  33. T cell-mediated lethal shock triggered in mice by the superantigen staphylococcal enterotoxin B: critical role of tumor necrosis factor. Miethke, T., Wahl, C., Heeg, K., Echtenacher, B., Krammer, P.H., Wagner, H. J. Exp. Med. (1992) [Pubmed]
  34. Protection from septic shock by neutralization of macrophage migration inhibitory factor. Calandra, T., Echtenacher, B., Roy, D.L., Pugin, J., Metz, C.N., Hültner, L., Heumann, D., Männel, D., Bucala, R., Glauser, M.P. Nat. Med. (2000) [Pubmed]
  35. Suramin inhibits death receptor-induced apoptosis in vitro and fulminant apoptotic liver damage in mice. Eichhorst, S.T., Krueger, A., Müerköster, S., Fas, S.C., Golks, A., Gruetzner, U., Schubert, L., Opelz, C., Bilzer, M., Gerbes, A.L., Krammer, P.H. Nat. Med. (2004) [Pubmed]
  36. Association of TNF2, a TNF-alpha promoter polymorphism, with septic shock susceptibility and mortality: a multicenter study. Mira, J.P., Cariou, A., Grall, F., Delclaux, C., Losser, M.R., Heshmati, F., Cheval, C., Monchi, M., Teboul, J.L., Riché, F., Leleu, G., Arbibe, L., Mignon, A., Delpech, M., Dhainaut, J.F. JAMA (1999) [Pubmed]
  37. Nitroglycerin in septic shock after intravascular volume resuscitation. Spronk, P.E., Ince, C., Gardien, M.J., Mathura, K.R., Oudemans-van Straaten, H.M., Zandstra, D.F. Lancet (2002) [Pubmed]
  38. Toxic shock syndrome: case-control studies at the Centers for Disease Control. Shands, K.N., Schlech, W.F., Hargrett, N.T., Dan, B.B., Schmid, G.P., Bennett, J.V. Ann. Intern. Med. (1982) [Pubmed]
 
WikiGenes - Universities