Evidence map›Paper›PMID 32854266›Full record

ArticleInternational journal of molecular sciences2020

Alteration of Colonic Mucosal Permeability during Antibiotic-Induced Dysbiosis.

Ying Ran, Hirokazu Fukui, Xin Xu, Xuan Wang, Nobuhiko Ebisutani, Yoshiki Tanaka, Ayako Maeda, Yutaka Makizaki, Hiroshi Ohno, Takashi Kondo and 5 more

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

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  20. ProbioticBiomedicines · 2021
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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

15 authors.

Ying RanDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Hyogo College of Medicine, 1-1, Mukogawa, Nishinomiya 663-8501, Japan.
Hirokazu FukuiDepartment of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China.
Xin XuDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Hyogo College of Medicine, 1-1, Mukogawa, Nishinomiya 663-8501, Japan.
Xuan WangDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Hyogo College of Medicine, 1-1, Mukogawa, Nishinomiya 663-8501, Japan.
Nobuhiko EbisutaniDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Hyogo College of Medicine, 1-1, Mukogawa, Nishinomiya 663-8501, Japan.
Yoshiki TanakaR&D Center, Biofermin Pharmaceutical Co., Ltd., 7-3-4, Higashi-machi, Ibukidai, Nishi-ku, Kobe 651-2242, Japan.
Ayako MaedaR&D Center, Biofermin Pharmaceutical Co., Ltd., 7-3-4, Higashi-machi, Ibukidai, Nishi-ku, Kobe 651-2242, Japan.
Yutaka MakizakiR&D Center, Biofermin Pharmaceutical Co., Ltd., 7-3-4, Higashi-machi, Ibukidai, Nishi-ku, Kobe 651-2242, Japan.
Hiroshi OhnoR&D Center, Biofermin Pharmaceutical Co., Ltd., 7-3-4, Higashi-machi, Ibukidai, Nishi-ku, Kobe 651-2242, Japan.
Takashi KondoDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Hyogo College of Medicine, 1-1, Mukogawa, Nishinomiya 663-8501, Japan.
Tomoaki KonoDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Hyogo College of Medicine, 1-1, Mukogawa, Nishinomiya 663-8501, Japan.
Katsuyuki TozawaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Hyogo College of Medicine, 1-1, Mukogawa, Nishinomiya 663-8501, Japan.
Toshihiko TomitaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Hyogo College of Medicine, 1-1, Mukogawa, Nishinomiya 663-8501, Japan.
Tadayuki OshimaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Hyogo College of Medicine, 1-1, Mukogawa, Nishinomiya 663-8501, Japan.ORCID 0000-0001-6949-932X
Hiroto MiwaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Hyogo College of Medicine, 1-1, Mukogawa, Nishinomiya 663-8501, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although dysbiosis is likely to disturb the mucosal barrier system, the mechanism involved has remained unclear. Here, we investigated alterations of colonic mucosal permeability and tight junction (TJ) molecules in mice with antibiotic-induced dysbiosis. Mice were orally administered vancomycin or polymyxin B for 7 days, and then fecal samples were subjected to microbial 16S rRNA analysis. The colonic mucosal permeability was evaluated by chamber assay. The colonic expression of TJ molecules and cytokines was examined by real-time RT-PCR, Western blotting, and immunohistochemistry. Caco2 cells were stimulated with cytokines and their transepithelial electric resistance (TEER) was measured. Vancomycin-treated mice showed significantly lower gut microbiota diversity than controls, and the same tendency was evident in polymyxin B-treated mice. The colonic mucosal permeability was significantly elevated in both vancomycin- and polymyxin B-treated mice. The expression of claudin 4 in the colonic mucosa was decreased in both vancomycin- and polymyxin B-treated mice. Colonic expression of

Indexed as

Administration, OralAnimalsAnti-Bacterial AgentsBacteriaCytokinesDisease Models, AnimalDysbiosisFecesHumansIntestinal MucosaMicePermeabilityPhylogenyPolymyxin BRNA, Ribosomal, 16SSequence Analysis, RNAAnti-Bacterial AgentsCytokinesPolymyxin BRNA, Ribosomal, 16STight Junction ProteinsVancomycinantibioticclaudincolorectalcytokinedysbiosisgut microbiomepermeabilitypolymyxin Btight junctionvancomycin

Identifiers

PMID32854266
PMCPMC7504080

What OpenQuestion holds

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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.