Medicinal importance of fungal beta-(1-->3), (1-->6)-glucans.
Non-cellulosic beta-glucans are now recognized as potent immunological activators, and some are used clinically in China and Japan. These beta-glucans consist of a backbone of glucose residues linked by beta-(1-->3)-glycosidic bonds, often with attached side-chain glucose residues joined by beta-(1-->6) linkages. The frequency of branching varies. The literature suggests beta-glucans are effective in treating diseases like cancer, a range of microbial infections, hypercholesterolaemia, and diabetes. Their mechanisms of action involve them being recognized as non-self molecules, so the immune system is stimulated by their presence. Several receptors have been identified, which include: dectin-1, located on macrophages, which mediates beta-glucan activation of phagocytosis and production of cytokines, a response co-ordinated by the toll-like receptor-2. Activated complement receptors on natural killer cells, neutrophils, and lymphocytes, may also be associated with tumour cytotoxicity. Two other receptors, scavenger and lactosylceramide, bind beta-glucans and mediate a series of signal pathways leading to immunological activation. Structurally different beta-glucans appear to have different affinities toward these receptors and thus generate markedly different host responses. However, the published data are not always easy to interpret as many of the earlier studies used crude beta-glucan preparations with, for the most part, unknown chemical structures. Careful choice of beta-glucan products is essential if their benefits are to be optimized, and a better understanding of how beta-glucans bind to receptors should enable more efficient use of their biological activities.
Chen
Jiezhong
J
Cancer Biology Program, Diamantia Institute for Cancer, Immunology and Metabolic Medicine, University of Queensland, Brisbane, Queensland 4102, Australia. jchen@cicr.uq.edu.au
Seviour
Robert
R
D000818:Animals; D002986:Clinical Trials as Topic; D003141:Communicable Diseases / Q000188:drug therapy; D016207:Cytokines / Q000096:biosynthesis / Q000378:metabolism; D003920:Diabetes Mellitus; D005658:Fungi / Q000737:chemistry*; D044882:Glucose Metabolism Disorders / Q000188:drug therapy; D006801:Humans; D006937:Hypercholesterolemia / Q000188:drug therapy; D007155:Immunologic Factors; D037181:Lectins, C-Type; D008214:Lymphocytes / Q000276:immunology / Q000378:metabolism; D008264:Macrophages / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D008565:Membrane Proteins / Q000378:metabolism; D009369:Neoplasms / Q000188:drug therapy; D009419:Nerve Tissue Proteins / Q000378:metabolism; D010587:Phagocytosis; D011956:Receptors, Cell Surface / Q000378:metabolism; D011951:Receptors, Complement / Q000378:metabolism; D015398:Signal Transduction; D013602:T-Lymphocytes, Cytotoxic / Q000378:metabolism; D051195:Toll-Like Receptor 2 / Q000378:metabolism; D047071:beta-Glucans / Q000737:chemistry / Q000276:immunology / Q000378:metabolism / Q000627:therapeutic use; D000099181:Dectin-1
D016207:Cytokines; D007155:Immunologic Factors; D037181:Lectins, C-Type; D008565:Membrane Proteins; D009419:Nerve Tissue Proteins; D011956:Receptors, Cell Surface; D011951:Receptors, Complement; D051195:Toll-Like Receptor 2; D047071:beta-Glucans; D000099181:Dectin-1