Evidence map›Paper›PMID 32055962›Full record

ArticleEuropean journal of nutrition2020

Gut microorganisms and their metabolites modulate the severity of acute colitis in a tryptophan metabolism-dependent manner.

Ji-Hee Shin, Young-Kwan Lee, Woo-Jeong Shon, Bora Kim, Che Ok Jeon, Joo-Youn Cho, Herbert C Morse, Eun Young Choi, Dong-Mi Shin

Abstract read
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In one paragraph

Article in European journal of nutrition, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.4field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 38 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Ji-Hee ShinDepartment of Food and Nutrition, Seoul National University College of Human Ecology, Seoul, 08826, Korea.
Young-Kwan LeeDepartment of Biomedical Sciences, Graduate School of Seoul National University, Seoul, 03080, Republic of Korea.
Woo-Jeong ShonDepartment of Food and Nutrition, Seoul National University College of Human Ecology, Seoul, 08826, Korea.
Bora KimDepartment of Clinical Pharmacology and Therapeutics, Seoul National University College of Medicine and Hospital, Seoul, 03080, Republic of Korea.
Che Ok JeonDepartment of Life Science, Chung-Ang University, 84 Huekseok-ro, Dongjak-gu, Seoul, 06974, Republic of Korea.
Joo-Youn ChoDepartment of Clinical Pharmacology and Therapeutics, Seoul National University College of Medicine and Hospital, Seoul, 03080, Republic of Korea.
Herbert C MorseVirology and Cellular Immunology Section, Laboratory of Immunogenetics, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, 20852, USA.
Eun Young ChoiDepartment of Biomedical Sciences, Graduate School of Seoul National University, Seoul, 03080, Republic of Korea. eycii@snu.ac.kr.
Dong-Mi ShinDepartment of Food and Nutrition, Seoul National University College of Human Ecology, Seoul, 08826, Korea. shindm@snu.ac.kr.
Seoul National University · KRSeoul National University Hospital · KRChung-Ang University · KRNational Institutes of Health · US

Funding

Ministry of Health and Welfare HI16C0047
6 · The paper itself

Abstract

purposeGrowing evidence shows that nutrient metabolism affects inflammatory bowel diseases (IBD) development. Previously, we showed that deficiency of indoleamine 2,3-dioxygenase 1 (Ido1), a tryptophan-catabolizing enzyme, reduced the severity of dextran sulfate sodium (DSS)-induced colitis in mice. However, the roles played by intestinal microbiota in generating the differences in disease progression between Ido1

methodsMicrobial 16s rRNA sequencing was conducted in Ido1

resultsMicrobiome analysis through 16S-rRNA gene sequencing showed that IDO1 deficiency increased intestinal bacteria that use tryptophan preferentially to produce indolic compounds. Urinary excretion of 3-indoxyl sulfate, a metabolized form of gut bacteria-derived indole, was significantly higher in Ido1

conclusionsOur results provide evidence that a genetic defect in utilizing tryptophan affects intestinal microbiota profiles, altering microbial metabolites, and colitis development. This suggests that the host and intestinal microbiota communicate through shared nutrient metabolic networks.

Indexed as

ColitisGastrointestinal MicrobiomeInflammatory Bowel DiseasesAnimalsDextran SulfateDisease Models, AnimalMiceMice, Inbred C57BLRNA, Ribosomal, 16STryptophanDextran SulfateRNA, Ribosomal, 16STryptophanColitisGut microbiotaIndoleIndoleamine 2,3-dioxygenase 1Tryptophan

Identifiers

PMID32055962
OpenAlexW3006075159

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.