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Lactic Acid Bacteria Isolated from Human Breast Milk Improve Colitis Induced by 2,4,6-Trinitrobenzene Sulfonic Acid by Inhibiting NF-κB Signaling in Mice

  • Kyung-Joo Kim (Department of Food and Nutrition, Eulji University) ;
  • Suhyun Kyung (Department of Research, GREEN CROSS Wellbeing Co., Ltd.) ;
  • Hui Jin (Department of Research, GREEN CROSS Wellbeing Co., Ltd.) ;
  • Minju Im (Department of Research, GREEN CROSS Wellbeing Co., Ltd.) ;
  • Jae-won Kim (Department of Research, GREEN CROSS Wellbeing Co., Ltd.) ;
  • Hyun Su Kim (BTC Corporation #906, Technology Development Centre) ;
  • Se-Eun Jang (Department of Food and Nutrition, Eulji University)
  • Received : 2023.03.15
  • Accepted : 2023.04.25
  • Published : 2023.08.28

Abstract

Inflammatory bowel disease (IBD), a chronic inflammatory disease, results from dysregulation of the immune responses. Some lactic acid bacteria (LAB), including Lactobacillus, alleviate IBD through immunomodulation. In this study, the anti-colitis effect of LAB isolated from human breast milk was investigated in a mouse model induced acute colitis with 2,4,6-trinitrobenzene sulfonic acid (TNBS). TNBS remarkably increased weight loss, colon shortening, and colonic mucosal proliferation, as well as the expression levels of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-1β. Oral administration of LAB isolated from human breast milk resulted in a reduction in TNBS-induced colon shortening, as well as induced cyclooxygenase (COX)-2, nitric oxide synthase (iNOS), nuclear factor-kappa B (NF-κB). In addition, LAB suppressed inflammatory cytokines such as TNF-α, IL-6, and IL-1β, and thus showed an effect of suppressing the level of inflammation induced by TNBS. Furthermore, LAB alleviated gut microbiota dysbiosis, and inhibited intestinal permeability by increasing the expression of intestinal tight junction protein including ZO-1. Collectively, these results suggest that LAB isolated from human breast milk can be used as a functional food for colitis treatment by regulating NF-κB signaling, gut microbiota and increasing expression of intestinal tight junction protein.

Keywords

Acknowledgement

This study was supported by GC Well-being.

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