ABOUT five out of 1,000 patients admitted to hospital develop bacterial sepsis leading to shock¹, the mortality rate for which is high despite antibiotic therapy². The infection results in hypotension and poor tissue perfusion, and eventually leads to the failure of several organ systems. Bacterial endotoxin is thought to be the direct cause of shock in Gram-negative sepsis, because it can cause shock in animals³, and antibodies against endotoxin prevent Gram-negative shock in animals⁴ and in humans^5–7. But, the symptoms of septic shock are the result of the actions of host cytokines induced by the endotoxin. The cytokiue interleukin-1 has been implicated as an important mediator of septic shock because it can induce tachycardia and hypotension and act synergistically with tumour necrosis factor to cause tissue damage⁸ and death⁹. We now report that a specific interleukin-1 receptor antagonist reduces the lethality of endotoxin-induced shock in rabbits, indicating that interleukin-1 does indeed play an important part in endotoxin shock.