Abstract
The mechanisms modulating host susceptibility to endotoxin are unknown. Evidence suggests that endotoxin pathophysiology is mediated in part by oxidative reactions that lead to tissue damage and organ failure. The proposition is that conditions which favour oxidation sensitise the host to endotoxin. Central to this hypothesis is that an increase in the polyunsaturated fatty-acid composition of membrane phospholipids enhances susceptibility because such fatty acids are easily oxidised to produce mediators of the endotoxic crisis. Cytokines, such as tumour-necrosis factor and interferon-gamma, may be ultimately responsible for orchestrating these changes and thereby modify the host response to endotoxin.