Evidence map›Paper›PMID 41583118›Full record

ArticleMediators of inflammation2026

Feihan Shen, Kewen Sun, Jianguo Song, Xueping Chen, Juan Dai, Ying Qi, Liwen Zhang, Liang Ma

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Mediators of inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Mediators of inflammation · 2026
    Article
  3. 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

8 authors.

Feihan ShenDepartment of Gastroenterology, The First People's Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China, suda.edu.cn.
Kewen SunDepartment of Gastroenterology, The First People's Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China, suda.edu.cn.
Jianguo SongDepartment of Gastroenterology, The Fifth People's Hospital of Xinjiang Uygur Autonomous Region, Xin Jiang, China.
Xueping ChenDepartment of Gastroenterology, The People's Hospital of Wuqia, Xin Jiang, China.
Juan DaiDepartment of Gastroenterology, The First People's Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China, suda.edu.cn.
Ying QiDepartment of Gastroenterology, The First People's Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China, suda.edu.cn.
Liwen ZhangDepartment of Pediatrics, the Second People's Hospital of Changzhou, The Third Affiliate Hospital of NanJing medical University, Changzhou, Jiangsu, China, njmu.edu.cn.ORCID https://orcid.org/0000-0002-9614-1216
Liang MaDepartment of Gastroenterology, The First People's Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China, suda.edu.cn.ORCID https://orcid.org/0000-0002-1979-5056

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Intestinal barrier dysfunction is a key driver of ulcerative colitis (UC) recurrence and chronic persistence. Modulating group 3 innate lymphoid cells (ILC3) activity and tryptophan-derived metabolites is crucial for enhancing mucosal repair in UC. Methods: Changes in body weight, food intake, DAI score, colon length, pathological score, and inflammatory factor level were performed to assess the therapeutic effect of RFELNs on DSS-stimulated UC mouse models. The effects of RFELNs on intestinal barrier integrity were assessed by intestinal barrier permeability analysis, Alcian Blue staining, immunohistochemistry (IHC), and western blot assays. IL-22 level was measured by immunofluorescent staining and ELISA assay. Besides, flow cytometry was performed to detect the proportions of ILC3 and NCR Results: RFELNs prominently relieved pathological symptoms in UC mice, including weight loss, enhanced DAI score, shortened colon, and pathological colon damage. Moreover, RFELNs decreased the concentration of FITC-dextran and DAO level and enhanced D-lactate levels. Additionally, RFELNs significantly enhanced the number of colonic goblet cells, restored epithelial tight junctions (TJs), and upregulated TJ protein levels. Moreover, RFELNs enhanced IL-22 expression and the proportion of ILC3 cells and NCR Conclusion: RFELNs restored intestinal barrier function in UC mice by activating AhR/IL-22 signaling through regulation of gut microbiota-dependent tryptophan metabolism.

Indexed as

Colitis, UlcerativeExosomesGastrointestinal MicrobiomeInterleukinsNanoparticlesReceptors, Aryl HydrocarbonTryptophanAnimalsFlowersInterleukin-22Intestinal Barrier FunctionIntestinal MucosaMaleMiceMice, Inbred C57BLInterleukin-22InterleukinsReceptors, Aryl HydrocarbonTryptophanAhRIL-22ILC3RFELNstryptophan metabolismUC

Identifiers

PMID41583118
PMCPMC12826113

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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.