Abstract
Summary Mice with a sublethal Histoplasma infection were shown to have an increased susceptibility to a bacterial endotoxin (S. typhosa, lipopolysaccharide). This increase in susceptibility was directly related to the degree of stimulation of the RES by the infection as reflected by change in liver size. Delayed hypersensitivity and increased susceptibility to endotoxin are separate phenomena as judged by their temporal relationships to the course of a sublethal Histoplasma infection. Although susceptibility to endotoxin declined as the organism count declined, delayed hypersensitivity to the homologous challenge remained at a high level when most of the organisms had been eliminated. On the other hand, both phenomena were inhibited by chemotherapy of the infection, and specific hypersensitivity was decreased by treatment with endotoxin.
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