Guar gum fiber increases suppressor of cytokine signaling-1 expression via toll-like receptor 2 and dectin-1 pathways, regulating inflammatory response in small intestinal epithelial cells

被引:16
|
作者
Tran Van Hung [1 ]
Suzuki, Takuya [1 ]
机构
[1] Hiroshima Univ, Grad Sch Biosphere Sci, Dept Biofunct Sci & Technol, Hiroshima, Japan
关键词
Dectin-1; Guar gum; Interleukin-8; Intestinal epithelium; Suppressor of cytokine signaling-1; Toll-like receptor 2; NECROSIS-FACTOR-ALPHA; MESSENGER-RNA STABILITY; SODIUM-INDUCED COLITIS; BARRIER FUNCTION; DIETARY FIBER; ACTIVATION; TRANSCRIPTION; INTERFERON; INDUCTION;
D O I
10.1002/mnfr.201700048
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Scope: Direct regulation of intestinal inflammation by intact dietary fibers is still unclear. Here, the anti-inflammatory regulation by intact guar gum (GG) was investigated using mice and human intestinal Caco-2 cells. Methods and results: Administration of dextran sodium sulfate (DSS) increased myeloperoxidase activity and CXC motif chemokine ligand2 (an IL-8 homolog) expression in the small intestines of mice, while supplemental GG reduced these increases. Stimulation of Caco-2 cells with tumor necrosis factor (TNF)-alpha induced IL-8 expression through nuclear factor kappa B p65, spleen tyrosine kinase, and mitogen-activated protein kinases pathways. Pre-treatment of cells with GG reduced the TNF-alpha-induced IL-8 expression and cellular signaling. GG increased the suppressor of cytokine signaling (SOCS)-1 expression in Caco-2 cells, suggesting that this is one of the probable mechanisms involved in GG-mediated anti-inflammatory regulation. The anti-inflammatory regulation and SOCS-1 expression induced by GG were sensitive to neutralization of toll-like receptor (TLR)2 and dectin-1, and to inhibition of Janus kinase (JAK) and tyrosine kinase cSrc pathways. Finally, supplemental GG increased SOCS-1 expression in the small intestines of both DSS-administered and normal mice. Conclusion: Intact GG activates TLR2 and dectin-1, and increases SOCS-1 expression via JAK and cSrc pathways, resulting in anti-inflammatory regulation in intestinal epithelium.
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页数:13
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