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

• Published in: Journal of microbiology and biotechnology Vol. 19; no. 6; pp. 616 - 621
• Main Authors: Lee, Bo-Mi, Lee, Jung-Hee, Lee, Hye-Sung, Bae, Eun-Ah, Huh, Chul-Sung, Ahn, Young-Tae, Kim, Dong-Hyun
• Format: Journal Article
• Language: Korean
• Published: 한국미생물생명공학회 30.06.2009
• Subjects: glycosaminoglycan; inflammatory bowel disease; intestinal bacteria; Lactic acid bacteria; TLR-4; Lactic acid bacteria; TLR-4; intestinal bacteria; glycosaminoglycan; inflammatory bowel disease
• ISSN: 1017-7825; 1738-8872

To evaluate the effects of lactic acid bacteria (LAB) in inflammatory bowel diseases (IBD), 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.