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Effects of Orally-Administered Bifidobacterium animalis subsp lactis Strain BB12 on Dextran Sodium Sulfate-Induced Colitis in Mice

Authors
Chae, Jung MinHeo, WanCho, Hyung TaekLee, Dong HunKim, Jun HoRhee, Min SukPark, Tae-SikKim, Yong KiLee, Jin HyupKim, Young Jun
Issue Date
11월-2018
Publisher
KOREAN SOC MICROBIOLOGY & BIOTECHNOLOGY
Keywords
Probiotics; colitis; TNF-alpha; apoptosis
Citation
JOURNAL OF MICROBIOLOGY AND BIOTECHNOLOGY, v.28, no.11, pp.1800 - 1805
Indexed
SCIE
SCOPUS
KCI
Journal Title
JOURNAL OF MICROBIOLOGY AND BIOTECHNOLOGY
Volume
28
Number
11
Start Page
1800
End Page
1805
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/71944
DOI
10.4014/jmb.1805.05072
ISSN
1017-7825
Abstract
Inflammatory bowel disease, including Crohn's disease and ulcerative colitis (UC), is a chronically relapsing inflammatory disorder of the gastrointestinal tract. Intestinal epithelial cells (IECs) constitute barrier surfaces and play a critical role in maintaining gut health. Dysregulated immune responses and destruction of IECs disrupt intestinal balance. Dextran sodium sulfate (DSS) is the most widely used chemical for inducing colitis in animals, and its treatment induces colonic inflammation, acute diarrhea, and shortening of the intestine, with clinical and histological similarity to human UC. Current treatments for this inflammatory disorder have poor tolerability and insufficient therapeutic efficacy, and thus, alternative therapeutic approaches are required. Recently, dietary supplements with probiotics have emerged as promising interventions by alleviating disturbances in the indigenous microflora in UC. Thus, we hypothesized that the probiotic Bifidobacterium animalis subsp. lactis strain BB12 could protect against the development of colitis in a DSS-induced mouse model of UC. In the present study, oral administration of BB12 markedly ameliorated DSS-induced colitis, accompanied by reduced tumor necrosis factor-alpha-mediated IEC apoptosis. These findings indicate that the probiotic strain BB12 can alleviate DSS-induced colitis and suggest a novel mechanism of communication between probiotic microorganisms and intestinal epithelia, which increases intestinal cell survival by modulating pro-apoptotic cytokine expression.
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