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Lactobacillus sakei K17, an inducer of IL-10 expression in antigen-presenting cells,attenuates TNBS-induced colitis in mice
Authors:Su-Hyeon Eun  Su-Min Lim  Se-Eun Jang  Myung Joo Han
Affiliation:1. Department of Life and Nanopharmaceutical Sciences, College of Pharmacy, Kyung Hee University, Seoul, Korea;2. Department of Food and Nutrition, Kyung Hee University, Seoul, Korea;3. Department of Food and Nutrition, Kyung Hee University, Seoul, Korea
Abstract:
To understand the anti-colitic effects of probiotics that up-regulate interleukin (IL)-10 expression in dendritic cells (DCs) and macrophages, we isolated Lactobacillus sakei K17, which potently induced IL-10 expression in DCs and peritoneal macrophages in vitro, among the lactic acid bacteria strains collected from kimchi and investigated its anti-inflammatory effect in mice with 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Oral administration of K17 (2?×?109 CFU·mouse?1·day?1) in mice with TNBS-induced colitis suppressed colon shortening and myeloperoxidase activity, as well as infiltration of CD86+?cells into the colon. Treatment with K17 also increased TNBS-suppressed expression of tight junction proteins and IL-10, but inhibited activation of nuclear factor-kappaB (NF-κB) and mitogen-activated protein kinases and expression of tumor necrosis factor α and IL-17. Its effect was comparable with that of sulfasalazine (50?mg/kg), a positive commercial ant-colitic drug. Furthermore, treatment with K17 (1?×?105 CFU/mL) potently inhibited lipopolysaccharide (LPS)-stimulated NF-κB activation in DCs and peritoneal macrophages and restored tight junction protein expression in LPS-stimulated Caco-2 cells. These findings suggest that Lactobacillus sakei K17 may ameliorate colitis by up-regulating the expression of IL-10 and tight junction proteins and inhibiting NF-κB activation.
Keywords:Colitis  dendritic cells  IL-10  inflammatory bowel disease  Lactobacillus sakei  macrophages
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