Evidence map›Paper›PMID 34294848›Full record

ArticleScientific reports2021

Clostridium butyricum enhances colonization resistance against Clostridioides difficile by metabolic and immune modulation.

Mao Hagihara, Tadashi Ariyoshi, Yasutoshi Kuroki, Shuhei Eguchi, Seiya Higashi, Takeshi Mori, Tsunemasa Nonogaki, Kenta Iwasaki, Makoto Yamashita, Nobuhiro Asai and 5 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
2.3field-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

48 citing papers in PubMed, 59 citations in OpenAlex.

  1. Trial
  2. Trial
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  4. Clinical analysis of 16 patients withNew microbes and new infections · 2026
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  11. Attenuation ofJournal of microbiology and biotechnology · 2026
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  15. iScience · 2025
    Article
  16. Article
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  18. Article
  19. Comparative genomics ofMicrobial genomics · 2025
    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

15 authors at 2 institutions in 1 country.

Mao HagiharaDepartment of Molecular Epidemiology and Biomedical Sciences, Aichi Medical University, Nagakute, 480-1195, Japan.
Tadashi AriyoshiDepartment of Clinical Infectious Diseases, Aichi Medical University, Nagakute, 480-1195, Japan.
Yasutoshi KurokiDepartment of Clinical Infectious Diseases, Aichi Medical University, Nagakute, 480-1195, Japan.
Shuhei EguchiMiyarisan Pharmaceutical Co., Ltd., Saitama, 114-0016, Japan.
Seiya HigashiMiyarisan Pharmaceutical Co., Ltd., Saitama, 114-0016, Japan.
Takeshi MoriDepartment of Clinical Infectious Diseases, Aichi Medical University, Nagakute, 480-1195, Japan.
Tsunemasa NonogakiDepartment of Pharmacy, College of Pharmacy, Kinjo Gakuin University, Nagoya, 463-8521, Japan.
Kenta IwasakiDepartments of Kidney Disease and Transplant Immunology, Aichi Medical University, Nagakute, 480-1195, Japan.
Makoto YamashitaDepartment of Clinical Infectious Diseases, Aichi Medical University, Nagakute, 480-1195, Japan.
Nobuhiro AsaiDepartment of Clinical Infectious Diseases, Aichi Medical University, Nagakute, 480-1195, Japan.
Yusuke KoizumiDepartment of Clinical Infectious Diseases, Aichi Medical University, Nagakute, 480-1195, Japan.
Kentaro OkaDepartment of Clinical Infectious Diseases, Aichi Medical University, Nagakute, 480-1195, Japan.
Motomichi TakahashiDepartment of Clinical Infectious Diseases, Aichi Medical University, Nagakute, 480-1195, Japan.
Yuka YamagishiDepartment of Clinical Infectious Diseases, Aichi Medical University, Nagakute, 480-1195, Japan.
Hiroshige MikamoDepartment of Clinical Infectious Diseases, Aichi Medical University, Nagakute, 480-1195, Japan. mikamo@aichi-med-u.ac.jp.
Aichi Medical University · JPKinjo Gakuin University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clostridioides difficile infection (CDI) represents the leading cause of nosocomial diarrhea worldwide and is associated with gut dysbiosis and intestinal damage. Clostridium butyricum MIYAIRI 588 (CBM 588) contributes significantly to reduce epithelial damage. However, the impacts of CBM 588 on antibacterial therapy for CDI are not clear. Here we show that CBM 588 enhanced the antibacterial activity of fidaxomicin against C. difficile and negatively modulated gut succinate levels to prevent C. difficile proliferation and downregulate tumor necrosis factor-α (TNF-α) producing macrophages in the colon lumina propria (cLP), resulting in a significant decrease in colon epithelial damage. Additionally, CBM 588 upregulated T cell-dependent pathogen specific immunoglobulin A (IgA) via interleukin (IL)-17A producing CD4

Indexed as

AntibiosisEnergy MetabolismImmunomodulationAnimalsAnti-Bacterial AgentsClostridioides difficileClostridium butyricumClostridium InfectionsDisease Models, AnimalDisease SusceptibilityFemaleGastrointestinal MicrobiomeImmunoglobulin AInterleukin-17MiceModels, BiologicalAnti-Bacterial AgentsIL17A protein, humanImmunoglobulin AInterleukin-17

Identifiers

PMID34294848
PMCPMC8298451
OpenAlexW3184987264

What OpenQuestion holds

Textmetadata
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.