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
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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.
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.
참고문헌 (29)
- Jeong JH, "Microvasculature remodeling in the mouse lower gut during inflammaging", Sci. Rep, 7, pp.39848~ (2017)
- Jeong JJ, "Orally administrated Lactobacillus pentosus var. plantarum C29ameliorates age-dependent colitis by inhibiting the nuclear factor-kappa B signaling pathway via the regulation of lipopolysaccharide production by gut microbiota", PLoS One, 10, pp.e0116533~ (2015)
- Park SH, "A 30-year trend analysis in the epidemiology of inflammatory bowel disease in the Songpa-Kangdong district of Seoul, Korea in 1986-2015", J. Crohns. Colitis, 13, pp.1410~1417 (2019)
- Lonnfors S, "IBD and health-related quality of life: discovering the true impact", J. Crohns Colitis, 8, pp.1281~1286 (2014)
- Jin Soo Moon, "Clinical aspects and treatments for pediatric inflammatory bowel diseases", Intestinal research, 17(1), pp.17~23 (2019), 대한장연구학회[DOI]
- Kim JW, "Trends in health-care costs and utilization for inflammatory bowel disease from 2010 to 2014 in Korea: a nationwide population-based study", J. Gastroenterol. Hepatol, 33, pp.847~854 (2018)
- Neuman MG, "Inflammatory bowel disease: role of diet, microbiota, life style", Trans. Res, 160, pp.29~44 (2012)
- Shanahan F, "Gut flora in gastrointestinal disease", Eur. J. Surg. Suppl, 587, pp.47~52 (2002)
- Ahuja V, "Inflammatory bowel disease in the Asia-Pacific area: a comparison with developed countries and regional differences", J. Dig. Dis, 11, pp.134~147 (2010)
- Marteau P, "Side effects of 5-aminosalicylic acid", Gastroenterol. Clin. Biol, 21, pp.377~386 (1997)
- Collins MP, "Probiotics, prebiotics, and synbiotics: approaches for modulating the microbial ecology of the gut", Am. J. Clin. Nutr, 69, pp.s1052~s1057 (1999)
- Paveljšek D, "Lactobacillus fermentum L930BB and Bifidobacterium animalis subsp. animalis IM386 initiate signalling pathways involved in intestinal epithelial barrier protection", Benef. Microbes, 9, pp.515~525 (2018)
- Peran L, "A comparative study of the preventative effects exerted by three probiotics, Bifidobacterium lactis, Lactobacillus casei and Lactobacillus acidophilus, in the TNBS model of rat colitis", J. Appl. Microbiol, 103, pp.836~844 (2007)
- 장세은, "Lactobacillus sakei S1 Improves Colitis Induced by 2,4,6-Trinitrobenzene Sulfonic Acid by the Inhibition of NF-κB Signaling in Mice", Journal of Microbiology and Biotechnology, 30(1), pp.71~78 (2020), 한국미생물·생명공학회
- Jang SE, "Lactobacillus plantarum CLP-0611 ameliorates colitis in mice by polarizing M1 to M2-like macrophages", Int. Immunopharmacol, 21, pp.186~192 (2014)
- Jang SE, "Amelioration of colitis in mice by Leuconostoc lactis EJ-1 by M1 to M2 macrophage polarization", Microbiol. Immunol, 64, pp.133~142 (2020)
- Fiorucci S, "Importance of innate immunity and collagen binding integrin alpha1beta1 in TNBS-induced colitis", Immunity, 17, pp.769~780 (2002)
- M F Neurath, "Predominant pathogenic role of tumor necrosis factor in experimental colitis in mice", Eur. J. Immunol, 27, pp.1743~1750 (1997)
- Fiorucci S, "Proteinase-activated receptor (PAR)-2 is an anti-inflammatory signal for colonic lamina propria lymphocytes in a mouse model of colitis", Proc. Natl. Acad. Sci. USA, 98, pp.13936~13941 (2001)
- Ruder B, "Tumour necrosis factor alpha in intestinal homeostasis and gut related diseases", Int. J. Mol. Sci, 20, pp.1887~ (2019)
- Min SW, "Anti-inflammatory effects of black rice, cyanidin-3-O-β-D-glycoside, and its metabolites, cyanidin and protocatechuic acid", Int. Immunopharmacol, 10, pp.959~966 (2010)
- Barens PJ, "Nuclear factor-kappaB: a pivotal transcription factor in chronic inflammatory diseases", N. Engl. J. Med, 336, pp.1066~1071 (1997)
- Collins T, "Transcriptional regulation of endothelial cell adhesion molecules: NF-κB and cytokine inducible enhancers", FASEB. J, 9, pp.899~909 (1995)
- 이성희, "Intestinal Permeability Regulation by Tight Junction: Implication on Inflammatory Bowel Diseases", Intestinal research, 13(1), pp.11~18 (2015), 대한장연구학회[DOI]
- Adlerberth I, "A mannose-specific adherence mechanism in Lactobacillus plantarum conferring binding to the human colonic cell line HT-29", Appl. Environ. Microbiol, 62, pp.2244~2251 (1996)
- Laparra JM, "Comparison of in vitro models to study bacterial adhesion to the intestinal epithelium", Lett. Appl. Microbiol, 49, pp.695~701 (2009)
- Arboleya S, "Characterization and in vitro properties of potentially probiotic Bifidobacterium strains isolated from breast-milk", Int. J. Food Microbiol, 149, pp.28~36 (2011)
- Sharma S, "Adherence potential of indigenous lactic acid bacterial isolates obtained from fermented foods of Western Himalayas to intestinal epithelial Caco-2 and HT-29 cell lines", J. Food Sci. Technol, 54, pp.3504~3511 (2017)
- Fava F, "Intestinal microbiota in inflammatory bowel disease: friend of foe?", World J. Gastroenterol, 7, pp.557~566 (2011)