Evidence map›Paper›PMID 38262747›Full record

ArticleInternational immunology2024

A purified diet affects intestinal epithelial proliferation and barrier functions through gut microbial alterations.

Hiroaki Shiratori, Kisara M Hattori, Kazuaki Nakata, Takuma Okawa, Seiga Komiyama, Yusuke Kinashi, Yuma Kabumoto, Yuria Kaneko, Motoyoshi Nagai, Tomoko Shindo and 6 more

Open access · hybridAbstract read
In one paragraph

Article in International immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
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

16 authors at 2 institutions in 1 country.

Hiroaki ShiratoriDivision of Biochemistry, Department of Pharmaceutical Sciences, Faculty of Pharmacy, and Graduate School of Pharmaceutical Sciences, Keio University, Minato-ku, Tokyo 105-8512, Japan.
Kisara M HattoriDivision of Biochemistry, Department of Pharmaceutical Sciences, Faculty of Pharmacy, and Graduate School of Pharmaceutical Sciences, Keio University, Minato-ku, Tokyo 105-8512, Japan.
Kazuaki NakataClinical Research Advancement Section, Research Institute, National Center for Global Health and Medicine, Tokyo 162-8655, Japan.
Takuma OkawaDivision of Biochemistry, Department of Pharmaceutical Sciences, Faculty of Pharmacy, and Graduate School of Pharmaceutical Sciences, Keio University, Minato-ku, Tokyo 105-8512, Japan.
Seiga KomiyamaDivision of Biochemistry, Department of Pharmaceutical Sciences, Faculty of Pharmacy, and Graduate School of Pharmaceutical Sciences, Keio University, Minato-ku, Tokyo 105-8512, Japan.
Yusuke KinashiDivision of Biochemistry, Department of Pharmaceutical Sciences, Faculty of Pharmacy, and Graduate School of Pharmaceutical Sciences, Keio University, Minato-ku, Tokyo 105-8512, Japan.
Yuma KabumotoDivision of Biochemistry, Department of Pharmaceutical Sciences, Faculty of Pharmacy, and Graduate School of Pharmaceutical Sciences, Keio University, Minato-ku, Tokyo 105-8512, Japan.
Yuria KanekoDivision of Biochemistry, Department of Pharmaceutical Sciences, Faculty of Pharmacy, and Graduate School of Pharmaceutical Sciences, Keio University, Minato-ku, Tokyo 105-8512, Japan.
Motoyoshi NagaiDivision of Biochemistry, Department of Pharmaceutical Sciences, Faculty of Pharmacy, and Graduate School of Pharmaceutical Sciences, Keio University, Minato-ku, Tokyo 105-8512, Japan.
Tomoko ShindoElectron Microscope Laboratory, Keio University School of Medicine, Tokyo 160-8582, Japan.
Nobuko MoritokiElectron Microscope Laboratory, Keio University School of Medicine, Tokyo 160-8582, Japan.
Yuki I KawamuraClinical Research Advancement Section, Research Institute, National Center for Global Health and Medicine, Tokyo 162-8655, Japan.
Taeko DohiDivision of Biochemistry, Department of Pharmaceutical Sciences, Faculty of Pharmacy, and Graduate School of Pharmaceutical Sciences, Keio University, Minato-ku, Tokyo 105-8512, Japan.
Daisuke TakahashiDivision of Biochemistry, Department of Pharmaceutical Sciences, Faculty of Pharmacy, and Graduate School of Pharmaceutical Sciences, Keio University, Minato-ku, Tokyo 105-8512, Japan.
Shunsuke KimuraDivision of Biochemistry, Department of Pharmaceutical Sciences, Faculty of Pharmacy, and Graduate School of Pharmaceutical Sciences, Keio University, Minato-ku, Tokyo 105-8512, Japan.
Koji HaseDivision of Biochemistry, Department of Pharmaceutical Sciences, Faculty of Pharmacy, and Graduate School of Pharmaceutical Sciences, Keio University, Minato-ku, Tokyo 105-8512, Japan.ORCID 0000-0001-9550-2334
Keio University · JPNational Center for Global Health and Medicine · JP

Funding

Fuji Foundation for Protein Research JPMJSP2123National Center for Global Health and Medicine
6 · The paper itself

Abstract

The gut microbiota plays a crucial role in maintaining epithelial barrier function. Although multiple studies have demonstrated the significance of dietary factors on the gut microbiota and mucosal barrier function, the impact of a purified diet, which has long been used in various animal experiments, on intestinal homeostasis remains to be elucidated. Here, we compared the impact of two different types of diets, a crude diet and an AIN-93G-formula purified diet, on epithelial integrity and the gut microbiota. Purified diet-fed mice exhibited shorter villi and crypt lengths and slower epithelial turnover, particularly in the ileum. In addition, antimicrobial products, including REG3γ, were substantially decreased in purified diet-fed mice. Purified diet feeding also suppressed α1,2-fucosylation on the epithelial surface. Furthermore, the purified diet induced metabolic rewiring to fatty acid oxidation and ketogenesis. 16S ribosomal RNA gene sequencing of the ileal contents and mucus layer revealed distinct gut microbiota compositions between the purified and crude diet-fed mice. Purified diet feeding reduced the abundance of segmented filamentous bacteria (SFB), which potently upregulate REG3γ and fucosyltransferase 2 (Fut2) by stimulating group 3 innate lymphoid cells (ILC3s) to produce IL-22. These observations illustrate that the intake of a crude diet secures epithelial barrier function by facilitating SFB colonization, whereas a purified diet insufficiently establishes the epithelial barrier, at least partly owing to the loss of SFB. Our data suggest that the influence of purified diets on the epithelial barrier integrity should be considered in experiments using purified diets.

Indexed as

Gastrointestinal MicrobiomeAnimalsBacteriaCell ProliferationDietImmunity, InnateLymphocytesMiceepithelial barrier functionepithelial metabolismgut microbiotasegmented filamentous bacteria

Identifiers

PMID38262747
PMCPMC10989658
OpenAlexW4391151353

What OpenQuestion holds

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LicenceCC BY
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.