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Melatonin controls microbiota in colitis by goblet cell differentiation and antimicrobial peptide production through Toll-like receptor 4 signalling

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dc.contributor.author김승원-
dc.contributor.author천재희-
dc.contributor.author천재희-
dc.date.accessioned2020-04-13T16:47:11Z-
dc.date.available2020-04-13T16:47:11Z-
dc.date.issued2020-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/175510-
dc.description.abstractMicrobial dysbiosis has long been postulated to be associated with the pathogenesis of inflammatory bowel disease (IBD). Although evidence supporting the anti-colitic effects of melatonin have been accumulating, it is not clear how melatonin affects the microbiota. Herein, we investigated the effects of melatonin on the microbiome in colitis and identified involvement of Toll-like receptor (TLR) 4 signalling in the effects. Melatonin improved dextran sulfate sodium (DSS)-induced colitis and reverted microbial dysbiosis in wild-type (WT) mice but not in TLR4 knockout (KO) mice. Induction of goblet cells was observed with melatonin administration, which was accompanied by suppression of Il1b and Il17a and induction of melatonin receptor and Reg3β, an antimicrobial peptide (AMP) against Gram-negative bacteria. In vitro, melatonin treatment of HT-29 intestinal epithelial cells promotes mucin and wound healing and inhibits growth of Escherichia coli. Herein, we showed that melatonin significantly increases goblet cells, Reg3β, and the ratio of Firmicutes to Bacteriodetes by suppressing Gram-negative bacteria through TLR4 signalling. Our study suggests that sensing of bacteria through TLR4 and regulation of bacteria through altered goblet cells and AMPs is involved in the anti-colitic effects of melatonin. Melatonin may have use in therapeutics for IBD.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherNature Publishing Group-
dc.relation.isPartOfSCIENTIFIC REPORTS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleMelatonin controls microbiota in colitis by goblet cell differentiation and antimicrobial peptide production through Toll-like receptor 4 signalling-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentOthers-
dc.contributor.googleauthorSeung Won Kim-
dc.contributor.googleauthorSoochan Kim-
dc.contributor.googleauthorMijeong Son-
dc.contributor.googleauthorJae Hee Cheon-
dc.contributor.googleauthorYoung Sook Park-
dc.identifier.doi10.1038/s41598-020-59314-7-
dc.contributor.localIdA00656-
dc.contributor.localIdA04030-
dc.contributor.localIdA04030-
dc.contributor.localIdA04030-
dc.contributor.localIdA04030-
dc.relation.journalcodeJ02646-
dc.identifier.eissn2045-2322-
dc.identifier.pmid32042047-
dc.contributor.alternativeNameKim, Seung Won-
dc.contributor.affiliatedAuthor김승원-
dc.contributor.affiliatedAuthor천재희-
dc.contributor.affiliatedAuthor천재희-
dc.contributor.affiliatedAuthor천재희-
dc.contributor.affiliatedAuthor천재희-
dc.citation.volume10-
dc.citation.number1-
dc.citation.startPagee2232-
dc.identifier.bibliographicCitationSCIENTIFIC REPORTS, Vol.10(1) : e2232, 2020-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Others (기타) > 1. Journal Papers

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