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1. (CSDB ID: 24821) | report error |
| -4)-b-D-ManpA-(1- | Show graphically |
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Pseudomonas aeruginosa O5
(Ancestor NCBI TaxID 287,
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]Little has been reported about the effects of different polysaccharides on cytokine production from human monocytes. In this study, we show that several well-defined polysaccharides, including polymers with different sizes of β 1-4-linked D-mannuronic acid (poly-M, high-M alginate, and M-blocks) and cellulose oxidized in the C-6 position, induced human monocytes to produce tumor necrosis factor alpha (TNF-α). Poly-M was the most efficient polysaccharide tested and, on a weight basis, was approximately as efficient as lipopolysaccharide (LPS) from Escherichia coli. TNF-α production was shown to depend strongly on the molecular weights of poly-M and high-M alginate, with maximal TNF-α production occurring at molecular weights above 50,000 and 200,000, respectively. G-blocks, α1-4-linked L-guluronic acid polymers that did not induce cytokine production from monocytes, reduced the cytokine production induced by the β 1-4-linked polyuronic acids and LPS. Furthermore, both G-blocks and LPS were found to inhibit the binding of poly-M to monocytes, as measured by flow cytometry. In addition, we found that the binding of LPS to monocytes was inhibited by G-blocks, M-blocks, and poly-M. Our results indicate that β 1-4-linked polyuronic acids and LPS may stimulate monocytes to produce TNF-α by similar mechanisms and may bind to a common receptor.
binding, alginate, tumor necrosis factor, cytokine, Monocytes
Structure type: homopolymer|
2. (CSDB ID: 45378) | report error |
| b-D-Glcp-(1-6)-+ b-D-Glcp-(1-6)-+ | | -3)-b-D-Glcp-(1-3)-b-D-Glcp-(1-3)-b-D-Glcp-(1-3)-b-D-Glcp-(1-3)-b-D-Glcp-(1- | Show graphically |
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Lentinus edodes
(later renamed to: Lentinula edodes)
(NCBI TaxID 5353,
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Activated human monocytes produce a monokine, interleukin-1 (IL-1) which can amplify the immune response by inducing antigen specific T cells to elaborate T cell growth factor, or interleukin-2, which in turn causes T cells to proliferate. The immune adjuvant lentinan has been shown in this study to augment IL-1 production by human monocytes. Stimulation of IL-1 by lentinan was seen as early as 5 hr, with some effect as late as 60 hr. Optimal effects were seen with very low concentrations, around 0.1 μg/ml. Lentinan was also able to stimulate IL-1 production by the leukemic cell line, K-562. The data reported here suggest that the previously reported adjuvant effects of lentinan may in part be mediated via its ability to stimulate IL-1 production.
macrophages, Monocytes, Immunotherapy, lentinan, Immunoadjuvants, lymphocyte proliferation, accessory cells, chronic myeloid leukemia, interleukin-1, K-562 cell line, phorbol myristate acetate
Structure type: structural motif or average structure|
3. (CSDB ID: 45414) | report error |
| b-D-Glcp-(1-6)-+ | -3)-b-D-Glcp-(1-3)-b-D-Glcp-(1-3)-b-D-Glcp-(1- | Show graphically |
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Schizophyllum commune
(NCBI TaxID 5334,
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We tested anti-tumor activities of macrophages treated with a neutral polysaccharide, schizophyllan (SPG), against syngeneic and allogeneic tumor cell lines. SPG was a macrophage stimulant which was not mitogenic to lymphocytes. That made a sharp contrast with the data that Corynebacterium parvum, BCG, and muramyl dipeptide (MDF) were macrophage stimulants which had lymphocyte-activating properties. Treatment of SPG-treated PEC with Thy12 monoclonal antibody and guinea pig complement did not affect the capabilities of tumor-cell-growth suppression by the treated PEC. Thus, the effector cells were peritoneal adherent cells (macrophages morphologically) and effector-to-target contact seemed to be necessary for effective tumor-cell-growth inhibition, although contradictory data exist for this. Murine peritoneal adherent cells harvested 4 days after a single IP injection of SPG at a dose of 100 mg/kg body weight of mouse showed the most prominent cytostatic and cytotoxic activities against syngeneic and allogeneic tumor cells. The distribution of anti-tumor activity in macrophages of various sizes followed the same pattern as macrophages treated with C. Parvum, i.e., larger macrophages showed more remarkable anti-tumor activity. Crude nonadherent peritoneal cells incubated with SPG at a concentration of 10 micrograms/ml, 100 micrograms/ml, or 1 mg/ml did not secrete lymphokine that rendered macrophages cytotoxic, while ConA-treated nonadherent cells did so. Furthermore, spleen cells treated with SPG in vivo did not secrete macrophage-activating lymphokine in the presence of SPG. On the other hand, addition of 1 mg/ml of SPG-treated peritoneal adherent cells and bone-marrow-derived macrophages in vitro rendered them cytotoxic to a moderate degree. This implies that SPG may activate macrophages directly, allowing them to become cytotoxic in the peritoneal cavity. Lastly, SPG could induce production of Il-1-like factor to a moderate degree. SPG, whose molecular structure is well elucidated, will provide us with a strong tool to analyze the mechanism of macrophage activation both in vitro and in vivo.
dipeptide, macrophage activation, tumor cell line, spleen cell, moderate degree
Structure type: polymer chemical repeating unit ; 400000-500000| New query | Export IDs | Home | Help |
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