Glycosaminoglycan Degradation-inhibitory Lactic Acid Bacteria Ameliorate 2,4,6-Trinitrobenzenesulfonic Acid-Induced Colitis in Mice

被引:28
|
作者
Lee, Bomi [1 ,2 ]
Lee, Jung-Hee [1 ,2 ,3 ]
Lee, Hye-Sung [1 ,2 ]
Bae, Eun-Ah [1 ,2 ]
Huh, Chul-Sung [3 ]
Ahn, Young-Tae [3 ]
Kim, Dong-Hyun [1 ,2 ]
机构
[1] Kyung Hee Univ, Dept Life & Nanopharmaceut Sci, Seoul 130701, South Korea
[2] Kyung Hee Univ, Dept Pharmaceut Sci, Seoul 130701, South Korea
[3] Korea Yakult Co Ltd, R&D Ctr, Yongin 446901, South Korea
关键词
Lactic acid bacteria; inflammatory bowel disease; glycosaminoglycan; TLR-4; intestinal bacteria; INFLAMMATORY-BOWEL-DISEASE; INTESTINAL FLORA; PROBIOTICS; ANTIBIOTICS; MICROFLORA; EXPRESSION; CYTOKINES;
D O I
10.4014/jmb.0808.479
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
To evaluate the effects of lactic acid bacteria (LAB) in inflammatory bowel diseases (M), we measured the inhibitory effect of several LAB isolated from intestinal microflora and commercial probiotics against the glycosaminoglycan (GAG) degradation by intestinal bacteria. Bifidobacterium longum HY8004 and Lactobacillus plantarum AK8-4 exhibited the most potent inhibition. These LAB inhibited colon shortening and myeloperoxidase production in 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced experimental colitic mice. These LAB also blocked the expression of the proinflammatory cytokines, IL-1 beta and TNF-alpha, as well as of COX-2, in the colon. LAB also blocked activation of the transcription factor, NF-kappa B, and expression of TLR-4 induced by TNBS. In addition, LAB reduced the TNBS-induced bacterial degradation activities of chondroitin sulfate and hyaluronic acid. These findings suggest that GAG degradation-inhibitory LAB may improve colitis by inhibiting inflammatory cytokine expression via TLR-4-linked NF-kappa B activation and by inhibiting intestinal bacterial GAG degradation.
引用
收藏
页码:616 / 621
页数:6
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