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Leukotrienes, Oxygen Radicals, and Cytokines in Septicemic Mice

  • A. Wendel
  • M. Niehörster
  • G. Tiegs
Conference paper
Part of the Colloquium der Gesellschaft für Biologische Chemie 11.–13. April 1991 in Mosbach/Baden book series (MOSBACH, volume 42)

Abstract

When microorganisms or certain parts of their cell walls invade a mammalian circulation system, the risk of the pathological state of sepsis arises. This situation is characterized by fever, blood pressure changes, and a general reaction of leukocytes. An overshoot reaction toward bacterial infection may lead to the life-threatening condition of septic shock, which even in modern intensive care units is difficult to clinically manage (Goris 1987). Under these given circumstances, the development of therapeutic strategies against septic shock is a primary research goal. The fulfillment of this need, however, depends on the availability and detailed mechanistic knowledge of the reactions involved in sepsis — an area to be explored in suitable model systems. Recent advances in the identification, isolation, and characterization of lipopolysaccharides (endotoxins), as the part of the cell wall of gram-negative bacteria responsible for inducing shock (Rietschel et al. 1983), allowed the induction of septicemic states in animals by administration of purified endotoxins. When this experimental protocol is applied, a dose-dependent increase in endotoxin-induced lethality is observed. An alternative to this all-or-none reaction model is also available: rodents can be sensitized to endotoxin several 1000-fold when they have been retreated with galactosamine. This amino sugar is metabolized exclusively in the liver, leads to an indirect protein biosynthesis block (Keppler and Decker 1969), and thus renders the liver as the prime target organ of endotoxin-induced injury (Galanos et al. 1979).

Keywords

Adult Respiratory Distress Syndrome Mouse Peritoneal Macrophage Suitable Model System Prime Target Organ Postischemic Tissue Injury 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag Berlin Heidelberg 1991

Authors and Affiliations

  • A. Wendel
    • 1
  • M. Niehörster
    • 1
  • G. Tiegs
    • 1
  1. 1.Biochemical PharmacologyUniversity of KonstanzKonstanzGermany

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