Abstract | BACKGROUND AND AIM: Bifidobacterium breve was the first bacteria isolated in the feces of healthy infants and is a dominant species in the guts of breast-fed infants. Some strains of B. breve have been shown to be effective at relieving intestinal inflammation, but the modes of action have yet to be elucidated. In this study, we investigated the mechanisms of action of B. breve CBT BR3 isolated from South Korean infant feces in relieving colitis in vitro and in vivo. METHODS: RESULTS: B. breve CBT BR3 was orally administered. B. breve CBT BR3 improved colitis symptoms in both DSS- and DNBS-induced colitis models. B. breve CBT BR3 increased the number of goblet cells per crypt. B. breve increased the mRNA expressions of Notch, Spdef, Muc5, and Il22. The mRNA expressions of Occludin, which encodes a membrane tight-junction protein, and Foxo3, which encodes a protein related to butyrate metabolism, were also increased in the DSS- and DNBS-induced colitis models. B. breve CBT BR3 protected inflammation-induced epithelial cell permeability and improved goblet cell function by inducing aryl hydrocarbon receptor in vitro. CONCLUSIONS: These results indicate that B. breve CBT BR3 is effective at relieving intestinal inflammation by augmenting goblet cell regeneration.
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Authors | I Seul Park, Ji Hyung Kim, Jongwook Yu, YooJin Shin, Kibeom Kim, Tae Il Kim, Seung Won Kim, Jae Hee Cheon |
Journal | Journal of gastroenterology and hepatology
(J Gastroenterol Hepatol)
Vol. 38
Issue 8
Pg. 1346-1354
(Aug 2023)
ISSN: 1440-1746 [Electronic] Australia |
PMID | 37157108
(Publication Type: Journal Article)
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Copyright | © 2023 Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd. |
Chemical References |
- Receptors, Aryl Hydrocarbon
- 2,4-dinitrofluorobenzene sulfonic acid
- RNA, Messenger
- Dextran Sulfate
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Topics |
- Humans
- Animals
- Mice
- Goblet Cells
(metabolism)
- Bifidobacterium breve
(genetics)
- Receptors, Aryl Hydrocarbon
(metabolism)
- Caco-2 Cells
- Colitis
(chemically induced, therapy, metabolism)
- Inflammation
(therapy, metabolism)
- RNA, Messenger
(genetics)
- Regeneration
- Dextran Sulfate
- Intestinal Mucosa
- Disease Models, Animal
- Mice, Inbred C57BL
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