Megalo-type α-1,6-glucosaccharides induce production of tumor necrosis factor α in primary macrophages via toll-like receptor 4 signaling
| Autor: | Hiroshi Hara, Atsuo Kimura, Masayuki Okuyama, Satoshi Ishizuka, Juri Sadahiro, Hidehisa Shimizu, Weeranuch Lang, Midori Andoh, Ga-Hyun Joe, Yuya Kumagai, Aki Shinoki |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Toll-like receptor biology Chemistry medicine.medical_treatment General Medicine General Biochemistry Genetics and Molecular Biology Cell biology 03 medical and health sciences 030104 developmental biology Immune system Cytokine biology.protein medicine TLR4 Macrophage Tumor necrosis factor alpha Interleukin 6 Lymphotoxin beta receptor |
| Zdroj: | Biomedical Research. 37:179-186 |
| ISSN: | 1880-313X 0388-6107 |
| DOI: | 10.2220/biomedres.37.179 |
| Popis: | The term "megalo-saccharide" is used for saccharides with ten or more saccharide units, whereas the term "oligo-saccharide" is used for saccharides containing fewer than ten monosaccharide units. Megalo-type α-1,6-glucosaccharide (M-IM) is a non-digestible saccharide and not utilized by intestinal bacteria, suggesting that ingested M-IM may encounter ileum Peyer's patches that contains immune cells such as macrophages. Macrophages are responsible for antigen incorporation and presentation during the initial step of immune responses. We investigated whether M-IMs modulate macrophage functions such as cytokine production, nitric oxide production, cell viability, and phagocytosis. Primary macrophages collected from the rats were cultured with the existence of M-IM or lipopolysaccharides (LPS). M-IM and LPS induced the production of tumor necrosis factor α (TNFα), interleukin 6 (IL6), and nitric oxide in the primary macrophages. The gene expression profile of inflammatory factors including TNFα, IL6, and ILlβ in M-IM-stimulated cells was similar to that of LPS-stimulated cells. The M-IM did not affect phagocytosis in the primary macrophages. The M-IM-induced TNFα production was suppressed in the cells treated with a tolllike receptor 4 (TLR4) inhibitor called TAK-242. In conclusion, the M-IM modulates cytokine expression via TLR4 signaling and may play a role in the modulation of immune responses. |
| Databáze: | OpenAIRE |
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