Activation of rat macrophages by Betafectin PGG-glucan requires cross-linking of membrane receptors distinct from complement receptor three (CR3)
| Autor: | William M. Mackin, Michael T Michalek, Kristen Lemerise, William Galbraith, David Melican, Myra L. Patchen, Matthew Langevin, Deborah Brunke-Reese |
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| Rok vydání: | 1998 |
| Předmět: |
Male
beta-Glucans Surface Properties Immunology Macrophage-1 Antigen macromolecular substances Complement receptor Saccharomyces cerevisiae Biology Cell Line Adjuvants Immunologic Cell surface receptor Superoxides Macrophages Alveolar Immunology and Allergy Animals Rats Wistar Receptors Immunologic Receptor Glucans Respiratory Burst Tumor Necrosis Factor-alpha PGG-glucan Cell Biology Macrophage Activation In vitro Cell biology Rats carbohydrates (lipids) stomatognathic diseases Biochemistry Solubility Cell culture Alveolar macrophage Tumor necrosis factor alpha Plastics |
| Zdroj: | Journal of leukocyte biology. 64(3) |
| ISSN: | 0741-5400 |
| Popis: | PGG-glucan (Betafectin ) is a soluble, highly purified yeast (1,3)-β-glucan with broad anti-infective and immunomodulatory activities. These studies evaluated the ability of PGG-glucan to directly elicit O2– and tumor necrosis factor α (TNF-α) production by rat leukocytes in vitro. Particulate β-glucan stimulated O2– production by the rat NR8383 alveolar macrophage cell line and resident rat peritoneal macrophages, but soluble PGG-glucan did not. In contrast, presentation of PGG-glucan to cells after covalent immobilization to a plastic surface caused a direct stimulation of O2– and TNF-α production. The O2– response of rat leukocytes to immobilized PGG-glucan was inhibited by soluble PGG-glucan, indicating that cellular responses to both immobilized and soluble PGG-glucan occur via common cell surface receptors. Because complement receptor type three (CR3) has been proposed as a β-glucan receptor on human leukocytes, NR8383 cells were evaluated for the presence of CR3. Indirect immunofluorescence and flow cytometric analysis showed that despite being responsive to both particulate and immobilized β-glucans, NR8383 cells expressed no detectable CR3. These results indicate that the β-glucan receptors on NR8383 cells are not CR3 and suggest that physical presentation plays an important role in inducing proinflammatory leukocyte responses to PGG-glucan. J. Leukoc. Biol. 64: 337–344; 1998. |
| Databáze: | OpenAIRE |
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