Role of spleen in endotoxin poisoning and reticuloendothelial function.

Abstract

The nature of cellular factors in host response to endotoxin was determined by studying various phases of reactivity to endotoxin in splenectomized and sham operated mice. Spleen ablation by itself actually increased the resistance of animals to endotoxin lethality and the absence of spleen did not interfere with either the development or expression of tolerance to the lethal effects of the toxin. The clearance rates of carbon and of endotoxin were normal after splenectomy and increased in conjunction with RES activation associated with endotoxin tolerance, both in sham operated and the splenectomized animals. From these results, it is concluded that subtle and specific adaptations of hepatic RE elements and/or critical metabolic functions play a determining role in endotoxicosis. Furthermore, the presence of spleen does not seem to be required for opsonization, phagocytosis and removal of either nonspecific, inert colloidal particles such as carbon, or of biological materials such as endotoxin. Pertinence of these findings to splenectomized patients is indicated.