Abstract
Septic shock has traditionally been recognised as a consequence of gram-negative bacteraemia, and only recently has it become clear that also gram-positive organisms cause this clinical syndrome. Various aspects of the pathophysiology of gram-negative bacteraemia-induced septic shock are increasingly understood. For example endotoxin, an LPS component of the gram-negative outer membrane, causes cells of the macrophage lineage to produce cytokines such as TNF and IL-1, either directly or by forming a complex with an acute-phase protein called LPS-binding protein (LBP). LPS-LBP complexes in turn represent ligands for the CD14 receptor on monocytes and macrophages. The acute and systemic release of large amounts of cytokines is associated with fatal outcome in human septic shock [1]. One of these cytokines, the macrophage product TNF-alpha, is regarded as the central mediator, since in animal models anti-TNF MAb given prophylactically before i.v. challenge with LPS is effective in preventing mortality [2, 3].
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© 1992 Springer-Verlag Berlin Heidelberg
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Wagner, H., Miethke, T., Heeg, K. (1992). Pathophysiology of T-Cell Mediated Shock Induced by Bacterial Superantigens. In: Mertelsmann, R. (eds) Lymphohaematopoietic Growth Factors in Cancer Therapy II. ESO Monographs. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-77801-8_2
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DOI: https://doi.org/10.1007/978-3-642-77801-8_2
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