epiglucan has been researched along with Communicable-Diseases* in 4 studies
2 review(s) available for epiglucan and Communicable-Diseases
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Beta-glucan: an ideal immunostimulant in aquaculture (a review).
The major hindrance in the development and sustainability of aquaculture industry is the occurrence of various diseases in the farming systems. Today, preventive and management measures are central concern to overcome such outbreak of diseases. Immunostimulants are considered as an effective tool for enhancing immune status of cultured organisms. Among different immunostimulants used in aquaculture practices, β-glucan is one of the promising immunostimulant, which is a homopolysaccharide of glucose molecule linked by the glycoside bond. It forms the major constituents of cell wall of some plants, fungi, bacteria, mushroom, yeast, and seaweeds. Major attention on β-glucan was captivated with the gain in knowledge on its receptors and the mechanism of action. The receptor present inside the animal body recognizes and binds to β-glucan, which in turn renders the animal with high resistance and enhanced immune response. This review highlights β-glucan as an immunostimulant, its effective dosages, and route of administration and furthermore provides an outline on role of β-glucan in enhancing growth, survival, and protection against infectious pathogens pertaining to fishes and shellfishes. Study also summarizes the effect of β-glucan on its receptors, recognition of proteins, immune-related enzymes, immune-related gene expression and their mechanisms of action. Topics: Adjuvants, Immunologic; Animals; Aquaculture; beta-Glucans; Communicable Diseases; Fish Diseases; Fishes; Gene Expression Regulation; Receptors, Immunologic; Shellfish | 2013 |
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. Topics: Animals; beta-Glucans; Clinical Trials as Topic; Communicable Diseases; Cytokines; Diabetes Mellitus; Fungi; Glucose Metabolism Disorders; Humans; Hypercholesterolemia; Immunologic Factors; Lectins, C-Type; Lymphocytes; Macrophages; Membrane Proteins; Neoplasms; Nerve Tissue Proteins; Phagocytosis; Receptors, Cell Surface; Receptors, Complement; Signal Transduction; T-Lymphocytes, Cytotoxic; Toll-Like Receptor 2 | 2007 |
2 other study(ies) available for epiglucan and Communicable-Diseases
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The rat antigen-presenting lectin-like receptor complex influences innate immunity and development of infectious diseases.
Genetic variation in the antigen-presenting lectin-like receptor gene complex (APLEC) associates with autoimmunity and arthritis in rats and humans. We hypothesized that the encoded C-type lectin-like receptors might influence innate immunity and responses to infectious agents. To test this hypothesis, we compared in vivo and in vitro phenotypes in DA rats and APLEC-congenic rats. Survival rates following infection with Staphylococcus aureus and Herpes simplex virus differed significantly between the two strains. Likewise, differential delayed type hypersensitivity (DTH), an immunological reaction involving T lymphocytes and macrophages, was observed in response to provocation with the chemical oxazolone. Unstimulated bone marrow-derived macrophages from the two strains appeared to already have polarized activation states with different mRNA levels of CD163 and Dectin-1 receptors. Following stimulation with a panel of microbial agents, differences in induced mRNA and protein levels were shown for interleukin (IL)-6 and IL-10 following stimulation with lipopolysaccharide, mannan and beta-glucan. Expression levels of APLEC gene mRNAs also differed, and both strains had a notably dichotomous expression of the genes, with general downregulation of all four Dcir genes and upregulation of Mincle and Mcl. We suggest that human APLEC genes may similarly regulate infectious diseases, DTH and general macrophage activation status. Topics: Adjuvants, Immunologic; Animals; Arthritis, Infectious; beta-Glucans; Cells, Cultured; Communicable Diseases; Cytokines; Encephalitis; Herpesvirus 1, Human; Hypersensitivity, Delayed; Immunity, Innate; Lectins, C-Type; Lipopolysaccharides; Macrophage Activation; Macrophages; Mannans; Oxazolone; Rats; Staphylococcal Infections; Staphylococcus aureus; Zymosan | 2009 |
Carbohydrate polymers: new immune system modifying agents for infectious diseases.
Topics: Adjuvants, Immunologic; beta-Glucans; Carbohydrates; Communicable Diseases; Glucans; Humans; Infections; Polymers | 1991 |