Bone Marrow Injury:
Daniel E Cramer, Daniel J Allendorf, Jarek T Baran, Richard Hansen, Jose Marroquin, Bing Li, Janina Ratajczak, Mariusz Z Ratajczak, and Jun Yan; “Beta-glucan enhances complement-mediated hematopoietic recovery after bone marrow injury;” Blood; DOI 10.1182. Tumor Immunobiology Program and Stem Cell Biology Program, James Graham Brown Cancer Center, University of Louisville, Louisville, KY, USA. Sept 2005.
Direct Quote: “…Myelotoxic injury in the bone marrow (BM) as a consequence of total body irradiation (TBI) or granulocyte colony stimulating factor (G-CSF) mobilization results in the deposition of iC3b on BM [bone marrow] stroma [cell framework]. … Taken together, these observations suggest a novel role for C, CR3, and Beta glucan in the restoration of hematopoiesis [cell formation] following injury.” NOTE: Mice were treated for 12 days with beta glucan and exposed to a sublethal dose of radiation. The beta glucan treated animals had approximately 40 percent more cell formation units in the spleen than untreated mice. When beta glucan was given orally, survival of animals receiving a lethal dose of radiation after stem cell transplantation was significantly enhanced. Forty days following radiation exposure, approximately 30 percent of mice treated with beta glucan survived compared with only 3 percent of untreated animals. Researchers discovered beta-glucan enhances the proliferation of stem cells, promoting white blood cell recovery in bone marrow injury and repair.
Hong F, Yan J, Baran JT, Allendorf DJ, Hansen RD, Ostroff G, Ross G, "Mechanism by Which Orally Administered B-1,3-Glucans Enhance the Tumoricidal Activity of Antitumor Monoclonal Antibodies in Murine Tumor Models," The J of Immunology 173:797-806. James Graham Brown Cancer Ctr, Louisville, KY; July 15, 2004:
Direct Quote: "Orally administered B-1,3-glucans were taken up by macrophages that transported them to spleen, lymph nodes, and bone marrow. Within the bone marrow, the macrophages degraded the large B-1,3 glucans into smaller soluble B-1,3-glucan fragments that were taken up by the CR3 [receptors] of marginated granulocytes [white blood cells formed in the bone marrow]. These granulocytes with CR3-bound B-1,3-glucan-fluorescein were shown to kill iC3b-opsonized tumor cells following their recruitment to a site of complement activation resembling a tumor coated with mAB [monoclonal antibodies]."
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