|
The following is a short list of important research on the Bracket fungi.
The chemical composition of the mushrooms annotated as “Bracket,” including Reishi, G. lucidum, and Tiaga, are very similar.
Here is some research on the mechanisms of action associated with 1:3, 1:6 beta-glucans.
Patchen M.L., McVittie T.J.; Temporal Response of Murine Pluripotent Stem Cells and Myeloid and Erythroid Progenitor Cells to Low-dose Glucan Treatment. Acta Hemat; 70:281-288. Experimental Hematology Dept, Armed Forces Radiobiology Research Insti, Bethesda, MD. 1983. Quote: "Clearly, there are numerous possible uses for an agent such as glucan, which is a potent stimulator of hemopoietic activity. Currently, we [U.S. Armed Services] are using glucan to enhance hemopoietic proliferation in conjunction with hemopoietic injury induced by radiation."
Todd, R.F.; "The Continuing Saga of Complement Receptor Type 3 (CR3)," J. Clin Invest.: Vol 98, 1-2. 1996. Div of Hematology/Oncology Dept of Int. Med, U of Michigan Med Ctr.* Quote: (p2) "In certain controlled clinical trials, the increased survival of patients receiving these immunostimulatory beta- glucans has been reported."
Williams D.L. ,et al ; "Pre-clinical Safety Evaluation of Soluble Glucan", Int. J. Immunophamac. Vol. 10, No. 4: 405-414. Dept of Phys, Tulane U Sch of Med, New Orleans, LA. 1988 Quote: "Soluble glucan, a beta-1,3-linked glucopyranose biological response modifier, is effective in the therapy of experimental neoplasia, infectious diseases and immune suppression."
Abel, G. and Czop, J.K., "Activation of Human Monocyte GM-CSF and TNF-. alpha. Production by Particulate Yeast Glucan," International Congress for Infectious Diseases, Montreal, Canada (abstract). 1990.* Dept of Medicine, Harvard Medical School, Boston, MA. Quote: "Beta-glucans are pharmacologic agents that rapidly enhance the host resistance to a variety of biologic insults through mechanisms involving macrophage activation."
Norton MD, JA [Prof of Surg, Chief of Endocrine and Oncologic Surgery]; "Editorial: Annals of Surgery," Washington University School of Medicine, Nov 1994. Quote: "In a prospective, randomized double-blind study, [Babineau, et.al.] demonstrate that the perioperative administration of PGG-glucan, a substance derived from yeast that increases the microbial killing activity of leukocytes, can decrease infectious complications in patients undergoing major surgical procedures...the preliminary results are positive and should be interpreted as good news."
Patchen M.L.; "Radioprotective effect of oral administration of beta-1,3-glucan," Armed Forces Radiobiology Research Institute, Bethesda, MD Research Report, 1989. Pachen ML, MacVittie TJ, "Comparative effects of soluble and particulate glucans on survival in irradiated mice," J Biol Response Mod 5(1):45-60. Experimental Hematology Dept, Armed Forces Radiobiology Research Inst, Bethesda, MD. Feb 1986. Quote: "Both glucan-P and glucan-F enhanced the recovery of peripheral blood white cell numbers, platelet numbers, and hematocrit values. In addition, both agents increased endogenous pluripotent hemopoietic stem cell numbers in sublethally irradiated mice."
Seljelid R , "A water-soluble aminated beta 1-3D-glucan derivative causes regression of solid tumors in mice," Biosci Rep 6(9):845-851. Sep 1986.* Quote: "When water-soluble aminated beta 1,-D-glucan (AG) was injected intravenously or intraperitoneally on day 7 of tumor growth, the tumors underwent complete regression."
Williams D.L. and DiLuzio N.R .; "Glucan-Induced Modification of murine Viral Hepatitis". Science (1980), 208: 67-69. 1980.* Quote: "Thus glucan is capable of increasing survival, inhibiting hepatic necrosis, and maintaining an activated state of phagocytic activity in mice challenged with [mouse hepatitis virus strain] MHV-A59."
Browder IW.,et al., "Protective Effect of Nonspecific Immunostimulation in Post Splenectomy Sepis". J. Surg. Res.; 35: 474-479. Dept of Surg and Physiol, Tulane U Sch of Med, LA. 1983. * Quote: "This study reports the use of glucan, a beta-1,3-polyglucose, as a nonspecific immunostimulant for postsplenectomy pneumococcal sepsis. ...Nonspecific immunostimulation appears to have significant potential as a treatment strategy against postplenectomy infection."
Czop, J.K., Valiante N.M., Janusz M.J.; "Phagocytosis of particulate activators of the human alternative complement pathway through monocyte beta-glucan receptors," Prog Clin Biol Res 297: 287-296; Dept of Med, Harvard Med S, Boston, MA. 1989. Quote (p1): "Animal studies indicate that beta-glucans with 1,3-and/or 1,6-linkages are active pharmacologic agents that rapidly confer protection to a normal host against a variety of biological insults. The beta-glucan receptors provide a mechanism by which a heightened state of host responsiveness is initiated."
DiLuzio N.R., "Immunopharmacology of glucan: a broad spectrum enhancer of host defense mechanisms," Trends in Pharmacol. SCI., 4:344-347. Dept of Physiology, Tulane U, New Orleans, LA.* 1983. Quote: (p347) "The broad spectrum of immunopharmacological activities of glucan includes not only the modification of certain bacterial, fungal, viral and parasitic infections, but also inhibition of tumor growth."
Hoffman OA, Olson EJ, Limper AH; Thoracic Disease Research Unit, Mayo Clinic, Rochester, MN 55905. “Tumor necrosis factor-alpha (TNF alpha) is a potent cytokine believed to participate in the development of endotoxin-induced shock and the adult respiratory distress syndrome. Treatment of animals with beta-glucan prior to bacterial challenge reduces TNF alpha release and prevents death. We therefore hypothesized that beta-glucan might regulate TNF alpha secretion from macrophages in response to lipopolysaccharide (LPS). Rat alveolar macrophages were cultured in the presence of beta-glucan alone and the TNF alpha secretion quantified using an L929 cytotoxicity assay. Concentrations of beta-glucan less than 500 micrograms/ml were found to stimulate TNF alpha release from macrophages. However, concentrations of beta-glucan greater than 500 micrograms/ml resulted in suppression of the TNF alpha activity released. This reduction in TNF alpha release was not mediated by a toxic effect of beta-glucan, as large concentrations of beta-glucan had no effect on macrophage viability. We further observed that the incubation of macrophages with large concentrations of beta-glucan (500 micrograms/ml) also inhibited the secretion of TNF alpha induced by bacterial LPS. Furthermore, interferon-gamma (IFN gamma), a potent activator of TNF alpha expression, failed to overcome the inhibition of TNF alpha caused by beta-glucan. These data suggest an immunomodulatory role for beta-glucan which may explain both the TNF alpha-stimulating and -inhibiting effects of fungal beta-glucans during infection.
|
