Use of glucan to enhance hemopoietic recovery after exposure to cobalt-60 irradiation.
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Biomedical subjects
Publications and source records attributed to M L Patchen.
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Inbred mouse strains C57BL/10Sn (Sn) and C57BL/10ScN (ScN) differ in response of their hematopoietic system to injection of lipopolysaccharide-W (LPS-W) in a manner similar to that observed for the LPS unresponsive C3H/HeJ and the paired responsive C3H/HeN strain mice. Responses of endogenous (E-CFU) stem cells as well as bone marrow and spleen-derived exogenous (CFU-s) stem cells, granulocyte-macrophage (GM-CFC) and macrophage (M-CFC) colony-forming cells were determined for Sn and ScN strain mice following an intraperitoneal injection of 10 micrograms LPS-W. Sn strain mice responded characteristically in terms of every parameter measured. Marrow-derived parameters reflected release of nucleated cells and early decrease of CFU-s, GM-CFC, and M-CFC followed by return toward control values. Peak splenic responses were observed within 4-5 days, whereas E-CFU increased significantly within 24 h after LPS-W. These responses were in marked contrast to those observed for the ScN strain mice, which were relatively unresponsive in terms of each parameter measured after LPS-W injection. These results show that the phenotypic expression of the defective LPS locus recently described in the ScN strain mice extends to those cells that control the response of the hematopoietic system to LPS, and is similar in every respect to those responses observed for the mutant LPS defective, C3H/HeJ strain mice.
We have investigated the mechanism of glucan-mediated increase of splenic (SPL) and decrease of bone marrow (BM) hemopoiesis in B6DF1 mice. To determine the involvement of macrophages in these phenomena, B6DF1 mice were treated with silica 24 hrs prior to glucan injection and then tested for BM and SPL CFU-GM and CFU-S activities. Silica treatment reduced significantly augmentation of SPL, but not the decrease of BM CFU-GM proliferation, indicating that the former phenomenon is macrophage dependent, whereas the latter is not. Since no change in BM or SPL CFU-S proliferation was observed after silica treatment, it appears that macrophages are not involved in glucan-caused alterations of CFU-S. Athymic mice (not possessing mature T cell functions) also exhibited decreased BM and increased SPL CFU-GM proliferation after glucan treatment; however, the SPL CFU-GM augmentation in athymic mice was not as dramatic. Hence, although glucan's action did not appear to be completely dependent on mature T-cells, these cells appear in some way to act with macrophages to enhance the proliferation of SPL CFU-GM after glucan treatment.
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