Evidence map›Paper›PMID 35039003›Full record

ArticleBMC gastroenterology2022

Intestinal Claudin-7 deficiency impacts the intestinal microbiota in mice with colitis.

Yuhan Ding, Kun Wang, Chang Xu, Mengdi Hao, Huimin Li, Lei Ding

Open access · goldAbstract read
In one paragraph

Article in BMC gastroenterology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Dysbiosis and extraintestinal cancers.Journal of experimental & clinical cancer research : CR · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. 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

6 authors at 3 institutions in 2 countries.

Yuhan DingDepartment of Oncology, Beijing Shijitan Hospital, Capital Medical University, Tieyilu 10, Yangfangdian, Haidian District, Beijing, 100038, China.
Kun WangDepartment of Oncology, Beijing Shijitan Hospital, Capital Medical University, Tieyilu 10, Yangfangdian, Haidian District, Beijing, 100038, China.
Chang XuDepartment of Oncology, Beijing Shijitan Hospital, Capital Medical University, Tieyilu 10, Yangfangdian, Haidian District, Beijing, 100038, China.
Mengdi HaoDepartment of Oncology, Beijing Shijitan Hospital, Capital Medical University, Tieyilu 10, Yangfangdian, Haidian District, Beijing, 100038, China.
Huimin LiDepartment of Oncology, Beijing Shijitan Hospital, Capital Medical University, Tieyilu 10, Yangfangdian, Haidian District, Beijing, 100038, China.
Lei DingDepartment of Oncology, Beijing Shijitan Hospital, Capital Medical University, Tieyilu 10, Yangfangdian, Haidian District, Beijing, 100038, China. dinglei1005@126.com.
Beijing Shijitan Hospital · CNCapital Medical University · CNMinistry of Education · ET

Funding

Beijing Municipal Natural Science Foundation 7192087National Natural Science Foundation of China 81772557
6 · The paper itself

Abstract

backgroundIntestinal epithelial cells form a physical barrier that protects the intestine against the intestinal microbiota through tight junctions (TJs) and adhesive junctions, while barrier disruption may lead to inflammatory bowel disease (IBD). Claudin-7 (Cldn7) has been implicated in this protection as an important member of TJs. Here, we experimentally study the effect of Cldn7 deletion on intestinal microbiota in colitis.

methodsColitis model was established based on inducible intestinal conditional Cldn7 gene knockout mice (Cldn7fl/fl; villin-CreERT2), by feeding with dextran sodium sulfate (DSS). AB-PAS staining and immunohistochemical staining of Muc2 mucin were used to detect the effect of Cldn7 deficiency on the mucus layer of mice with colitis, and fluorescence in situ hybridization was used to detect how Cldn7 promotes spatial separation of the gut microbiota from the host. The microbiota population was characterized by high-throughput 16S rRNA gene sequencing of DNA extracted from fecal samples.

resultsCompared with the controls, Cldn7 knockout increased susceptibility to colitis, including greater degree of weight loss, colon shortening, and a significantly higher disease activity index score. DSS-treated Cldn7 knockout mice promoted the migration of bacteria to the intestinal epithelium to some extent by damaging the intestinal mucus layer. Sequencing of 16S rRNA showed that DSS-treated Cldn7 knockout mice reduced the gut microbiota diversity and had greater relative abundance of Escherichia coli. LEfSe analysis indicated that Escherichia coli may be the key bacteria in Cldn7 knockout mice during DSS-induced colitis. Furthermore, the Tax4Fun analysis predicted that DSS-treated Cldn7 knockout mice enriched for microbiota impacting infectious diseases, immune system and metabolic functions.

conclusionsOur data suggests an association between intestinal Cldn7 knockout and microbiota dysbiosis during inflammatory events.

Indexed as

ColitisGastrointestinal MicrobiomeAnimalsClaudinsColonDextran SulfateDisease Models, AnimalIn Situ Hybridization, FluorescenceIntestinal MucosaMiceMice, Inbred C57BLMice, KnockoutRNA, Ribosomal, 16SClaudinsDextran SulfateRNA, Ribosomal, 16SClaudin-7ColitisIntestinal microbiotaMicrobiota dysbiosisTight junction

Identifiers

PMID35039003
PMCPMC8762895
OpenAlexW4205773137

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.