The seeding efficiency of colony‐forming cells from normal, regenerating and velocity‐sedimented cycling and non‐cycling narrow preparations was compared. Colony‐forming cells in cycle were found to exhibit a 50% reduction in splenic seeding when compared to normal marrow or sedimented non‐cycling cells. The results of this study indicate that the spleen colony assay underestimates the total number of colony‐forming cells by a fraction which is directly related to the number of cells in cycle.
The ability of a single injection of killed, intact bacteria to effect an increase in the proliferative rate of hemopoietic stem cells was studied. The total numbers of colony forming units in bone marrow, spleen and peripheral blood as well as the proportion of CFU in cycle was assessed. Splenic CFU were observed to rise exponentially due initially to in situ proliferation and later to proliferation in bone marrow with migration via the blood to the spleen. The results are discussed in the light of current concepts of stem cell regulation.
Summary.
Tritiated thymidine autoradiography was used to study the control of granulocyte production and release using the irradiated leg shielded mouse as an experimental model. Neutropenia resulted in a shortening of 24–36 hr in the mean transit time through the non‐proliferating granulocyte compartment. There was little difference between neutropenic and control animals in labelling indices of the cells in the proliferative granulocyte compartments, which suggests that the granulocytic hyperplasia observed in the neutropenic mice was predominantly due to differentiation of morphologically unrecognizable precursor cells rather than increased proliferation of morphologically recognizable cells. The persistence of a labelling index of approximately 60% in the myeloblast‐promyelocyte compartment 24 hr after injection suggests that these precursor cells were rapidly proliferating.
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