ABSTRACT
The phenomenon of endotoxin tolerance has attracted substantial attention, since it provides a host with increased resistance to endotoxin and to possibly unrelated assaults such as hemorrhagic shock. This chapter discusses the aspects of the new information with regard to cellular and molecular components that have been recognized to contribute to the early phase of endotoxin tolerance. Although the lethal effects of endotoxin are examined in this chapter, it is suggested that endotoxin tolerance is evident in mice in whom endogenous glucocorticoids are antagonized. Although the authors did not provide an explanation for the higher tumor necrosis factor (TNF) levels in tolerant rats, this finding is in agreement with the notion that endotoxin tolerance includes mechanisms that interfere with the activity of proinflammatory cytokines such as TNF. The studies reviewed in this chapter provide good evidence that endotoxin tolerance serves to protect against infection, tumor resistance, hemorrhagic shock, and myocardial ischemia/reperfusion injury.
