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Bacterial β-(1,3)-glucan prevents DSS-induced IBD by restoring the reduced population of regulatory T cells.
- Source :
-
Immunobiology [Immunobiology] 2014 Oct; Vol. 219 (10), pp. 802-12. Date of Electronic Publication: 2014 Jul 21. - Publication Year :
- 2014
-
Abstract
- Bacterial β-(1,3)-glucan has more advantages in terms of cost, yield and efficiency than that derived from mushrooms, plants, yeasts and fungi. We have previously developed a novel and high-yield β-(1,3)-glucan produced by Agrobacterium sp. R259. This study aimed to elucidate the functional mechanism and therapeutic efficacy of bacterial β-(1,3)-glucan in dextran sulfate sodium (DSS)-induced inflammatory bowel disease (IBD).Mice were orally pretreated with bacterial β-(1,3)-glucan at daily doses of 2.5 or 5mg/kg for 2 weeks. After 6 days of DSS treatment, clinical assessment of IBD severity and expression of pro-inflammatory cytokines were evaluated. In vivo cell proliferation was examined by immunohistochemistry using Ki-67 and ER-TR7 antibodies. The frequency of regulatory T cells (Tregs) was analyzed by flow cytometry. Natural killer (NK) activity and IgA level were evaluated using NK cytotoxicity assay and ELISA.The deterioration of body weight gain, colonic architecture, disease score and histological score was recovered in DSS-induced IBD mice when pretreated with bacterial β-(1,3)-glucan. The recruitment of macrophages and the gene expression of proinflammatory cytokines, such as IL-1β, IL-6 and IL-17A/F, were markedly decreased in the colon of β-(1,3)-glucan-pretreated mice. β-(1,3)-Glucan induced the recovery of Tregs in terms of their frequency in DSS-induced IBD mice. Intriguingly, β-(1,3)-glucan reversed the functional defects of NK cells and excessive IgA production in DSS-induced IBD mice.We conclude that bacterial β-(1,3)-glucan prevented the progression of DSS-induced IBD by recovering the reduction of Tregs, functional defect of NK cells and excessive IgA production.<br /> (Copyright © 2014 Elsevier GmbH. All rights reserved.)
- Subjects :
- Agrobacterium metabolism
Animals
Anti-Inflammatory Agents metabolism
Anti-Inflammatory Agents pharmacology
Cell Proliferation drug effects
Colon cytology
Colon pathology
Cytokines genetics
Dextran Sulfate
Epithelial Cells cytology
Epithelial Cells drug effects
Feces chemistry
Fibroblasts cytology
Fibroblasts drug effects
Gene Expression drug effects
Immunoglobulin A immunology
Inflammatory Bowel Diseases chemically induced
Inflammatory Bowel Diseases immunology
Inflammatory Bowel Diseases pathology
Killer Cells, Natural immunology
Lymph Nodes cytology
Male
Mice, Inbred C57BL
Proteoglycans
Reactive Oxygen Species immunology
beta-Glucans metabolism
beta-Glucans pharmacology
Anti-Inflammatory Agents therapeutic use
Inflammatory Bowel Diseases drug therapy
T-Lymphocytes, Regulatory immunology
beta-Glucans therapeutic use
Subjects
Details
- Language :
- English
- ISSN :
- 1878-3279
- Volume :
- 219
- Issue :
- 10
- Database :
- MEDLINE
- Journal :
- Immunobiology
- Publication Type :
- Academic Journal
- Accession number :
- 25092569
- Full Text :
- https://doi.org/10.1016/j.imbio.2014.07.003