Evidence map›Paper›PMID 32345659›Full record

ArticleLife science alliance2020

Paneth cell α-defensin misfolding correlates with dysbiosis and ileitis in Crohn's disease model mice.

Yu Shimizu, Kiminori Nakamura, Aki Yoshii, Yuki Yokoi, Mani Kikuchi, Ryuga Shinozaki, Shunta Nakamura, Shuya Ohira, Rina Sugimoto, Tokiyoshi Ayabe

Open access · goldAbstract read
In one paragraph

Article in Life science alliance, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. A Novel Mixture ContainingInternational journal of molecular sciences · 2026
    Article
  3. Article
  4. Epithelial and stromal remodeling in murine Crohn's disease-like ileitis.bioRxiv : the preprint server for biology · 2025
    Article
  5. Article
  6. Article
  7. Inflammation induced by the new lineage ofFrontiers in immunology · 2025
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Crohn's disease: Why the ileum?World journal of gastroenterology · 2023
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

10 authors at 1 institution in 1 country.

Yu ShimizuInnate Immunity Laboratory, Graduate School of Life Science, Hokkaido University, Hokkaido, Japan.ORCID 0000-0002-5439-7678
Kiminori NakamuraInnate Immunity Laboratory, Graduate School of Life Science, Hokkaido University, Hokkaido, Japan.
Aki YoshiiInnate Immunity Laboratory, Graduate School of Life Science, Hokkaido University, Hokkaido, Japan.
Yuki YokoiInnate Immunity Laboratory, Graduate School of Life Science, Hokkaido University, Hokkaido, Japan.ORCID 0000-0002-8077-3200
Mani KikuchiDepartment of Cell Biological Science, Faculty of Advanced Life Science, Hokkaido University, Hokkaido, Japan.
Ryuga ShinozakiInnate Immunity Laboratory, Graduate School of Life Science, Hokkaido University, Hokkaido, Japan.
Shunta NakamuraInnate Immunity Laboratory, Graduate School of Life Science, Hokkaido University, Hokkaido, Japan.
Shuya OhiraInnate Immunity Laboratory, Graduate School of Life Science, Hokkaido University, Hokkaido, Japan.ORCID 0000-0003-4326-9707
Rina SugimotoInnate Immunity Laboratory, Graduate School of Life Science, Hokkaido University, Hokkaido, Japan.
Tokiyoshi AyabeInnate Immunity Laboratory, Graduate School of Life Science, Hokkaido University, Hokkaido, Japan ayabe@sci.hokudai.ac.jp.ORCID 0000-0002-8631-5593
Hokkaido University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Crohn's disease (CD) is an intractable inflammatory bowel disease, and dysbiosis, disruption of the intestinal microbiota, is associated with CD pathophysiology. ER stress, disruption of ER homeostasis in Paneth cells of the small intestine, and α-defensin misfolding have been reported in CD patients. Because α-defensins regulate the composition of the intestinal microbiota, their misfolding may cause dysbiosis. However, whether ER stress, α-defensin misfolding, and dysbiosis contribute to the pathophysiology of CD remains unknown. Here, we show that abnormal Paneth cells with markers of ER stress appear in SAMP1/YitFc, a mouse model of CD, along with disease progression. Those mice secrete reduced-form α-defensins that lack disulfide bonds into the intestinal lumen, a condition not found in normal mice, and reduced-form α-defensins correlate with dysbiosis during disease progression. Moreover, administration of reduced-form α-defensins to wild-type mice induces the dysbiosis. These data provide novel insights into CD pathogenesis induced by dysbiosis resulting from Paneth cell α-defensin misfolding and they suggest further that Paneth cells may be potential therapeutic targets.

Indexed as

Protein Foldingalpha-DefensinsAnimalsBacteroidaceaeBacteroidetesCrohn DiseaseDisease Models, AnimalDisease ProgressionDysbiosisEndoplasmic ReticulumEndoplasmic Reticulum StressFecesGastrointestinal MicrobiomeIleitisIleumMicealpha-DefensinsRNA, Ribosomal, 16S

Identifiers

PMID32345659
PMCPMC7190275
OpenAlexW3018465104

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.