Evidence map›Paper›PMID 31727909›Full record

ArticleScientific reports2019

High-fat diet-mediated dysbiosis exacerbates NSAID-induced small intestinal damage through the induction of interleukin-17A.

Naoki Sugimura, Koji Otani, Toshio Watanabe, Geicho Nakatsu, Sunao Shimada, Kosuke Fujimoto, Yuji Nadatani, Shuhei Hosomi, Fumio Tanaka, Noriko Kamata and 5 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Microbial threads in the tapestry of rheumatoid arthritis.The Journal of clinical investigation · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Prominent Indomethacin-Induced Enteropathy in FcgriibInternational journal of molecular sciences · 2021
    Article
  11. Gut Microbiota in NSAID Enteropathy: New Insights From Inside.Frontiers in cellular and infection microbiology · 2021
    Review
  12. Article
  13. Article
  14. NSAID-Gut Microbiota Interactions.Frontiers in pharmacology · 2020
    Review
  15. Review
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

15 authors at 2 institutions in 2 countries.

Naoki SugimuraDepartment of Gastroenterology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka, 545-8585, Japan.
Koji OtaniDepartment of Gastroenterology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka, 545-8585, Japan.ORCID http://orcid.org/0000-0001-9075-6415
Toshio WatanabeDepartment of Gastroenterology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka, 545-8585, Japan. watanabet@med.osaka-cu.ac.jp.
Geicho NakatsuDepartment of Immunology and Infectious Diseases/Genetics and Complex Diseases, Harvard T. H. Chan School of Public Health, Room 904, Building 1, 665 Huntington Avenue, Boston, Massachusetts, 02115, United States.
Sunao ShimadaDepartment of Gastroenterology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka, 545-8585, Japan.
Kosuke FujimotoDepartment of Immunology and Genomics, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka, 545-8585, Japan.
Yuji NadataniDepartment of Gastroenterology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka, 545-8585, Japan.
Shuhei HosomiDepartment of Gastroenterology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka, 545-8585, Japan.
Fumio TanakaDepartment of Gastroenterology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka, 545-8585, Japan.
Noriko KamataDepartment of Gastroenterology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka, 545-8585, Japan.
Koichi TairaDepartment of Gastroenterology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka, 545-8585, Japan.
Yasuaki NagamiDepartment of Gastroenterology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka, 545-8585, Japan.
Tetsuya TanigawaDepartment of Gastroenterology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka, 545-8585, Japan.
Satoshi UematsuDepartment of Immunology and Genomics, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka, 545-8585, Japan.
Yasuhiro FujiwaraDepartment of Gastroenterology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka, 545-8585, Japan.
Osaka City University · JPHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs) cause damage in the small intestine in a bacteria-dependent manner. As high-fat diet (HFD) is a potent inducer of gut dysbiosis, we investigated the effects of HFD on bacterial flora in the small intestine and NSAID-induced enteropathy. 16S rRNA gene analysis revealed that the population of Bifidobacterium spp. significantly decreased by fold change of individual operational taxonomic units in the small intestine of mice fed HFD for 8 weeks. HFD increased intestinal permeability, as indicated by fluorescein isothiocyanate-dextran absorption and serum lipopolysaccharide levels, accompanied by a decrease in the protein expressions of ZO-1 and occludin and elevated mRNA expression of interleukin (IL)-17A in the small intestine. HFD-fed mice exhibited increased susceptibility to indomethacin-induced damage in the small intestine; this phenotype was observed in normal diet-fed mice that received small intestinal microbiota from HFD-fed mice. Administration of neutralizing antibodies against IL-17A to HFD-fed mice reduced intestinal permeability and prevented exacerbation of indomethacin-induced damage. Thus, HFD-induced microbial dysbiosis in small intestine caused microinflammation through the induction of IL-17A and increase in intestinal permeability, resulting in the aggravation of NSAID-induced small intestinal damage.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalBifidobacteriumDextransDiet, High-FatDisease Models, AnimalDysbiosisFluorescein-5-isothiocyanateIndomethacinInterleukin-17Intestine, SmallLipopolysaccharidesMaleMiceMice, Inbred C57BLPermeabilityAnti-Inflammatory Agents, Non-SteroidalDextransFluorescein-5-isothiocyanatefluorescein isothiocyanate dextranIl17a protein, mouseIndomethacinInterleukin-17LipopolysaccharidesRNA, Ribosomal, 16S

Identifiers

PMID31727909
PMCPMC6856170
OpenAlexW2986316313

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.