Multiple doses of S. typhosa endotoxin caused an increase in the number of hemopoietic stem cells present in mouse marrow and spleen that could be detected using the spleen‐colony assay. This increase was inhibited by Colcemid, and by the genetically‐determined defect in hemopoiesis in mice of genotype S1/S1 d . However, the defect in S1/S1 d hosts did not prevent an endotoxin‐induced increase in the number of cells capable of forming colonies in cell culture. The results support the view that bacterial endotoxin acts, via a genetically‐controlled regulatory mechanism, to stimulate the proliferation of hemopoietic stem cells in the spleen.
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McCulloch et al. (1970) studied this question.
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