Bacterial β-(1,3)-glucan prevents DSS-induced IBD by restoring the reduced population of regulatory T cells.

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.

• Authors: Kwang-Ho Lee, Min Park, Kon-Young Ji, Hwa-Youn Lee, Ji-Hun Jang, Il-Joo Yoon, Seung-Su Oh, Su-Man Kim, Yun-Hwa Jeong, Chul-Ho Yun, Mi-Kyoung Kim, In-Young Lee, Ha-Rim Choi, Ki-sung Ko, Hyung-Sik Kang
• Journal: Immunobiology (Immunobiology) Vol. 219 Issue 10 Pg. 802-12 (Oct 2014) ISSN: 1878-3279 [Electronic] Netherlands
• PMID: 25092569 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2014 Elsevier GmbH. All rights reserved.

Chemical References

• Anti-Inflammatory Agents
• Cytokines
• Immunoglobulin A
• Proteoglycans
• Reactive Oxygen Species
• beta-Glucans
• polysaccharide-K
• Dextran Sulfate

Topics

• Agrobacterium (metabolism)
• Animals
• Anti-Inflammatory Agents (metabolism, pharmacology, therapeutic use)
• Cell Proliferation (drug effects)
• Colon (cytology, pathology)
• Cytokines (genetics)
• Dextran Sulfate
• Epithelial Cells (cytology, drug effects)
• Feces (chemistry)
• Fibroblasts (cytology, drug effects)
• Gene Expression (drug effects)
• Immunoglobulin A (immunology)
• Inflammatory Bowel Diseases (chemically induced, drug therapy, immunology, pathology)
• Killer Cells, Natural (immunology)
• Lymph Nodes (cytology)
• Male
• Mice, Inbred C57BL
• Proteoglycans
• Reactive Oxygen Species (immunology)
• T-Lymphocytes, Regulatory (immunology)
• beta-Glucans (metabolism, pharmacology, therapeutic use)