Evidence map›Paper›PMID 25799939›Full record

ArticleDigestive diseases and sciences2015

Aryl Hydrocarbon Receptor Activation Down-Regulates IL-7 and Reduces Inflammation in a Mouse Model of DSS-Induced Colitis.

Tao Ji, Chao Xu, Lihua Sun, Min Yu, Ke Peng, Yuan Qiu, Weidong Xiao, Hua Yang

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Article in Digestive diseases and sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
4.7field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

58 citing papers in PubMed, 83 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Tao JiDepartment of General Surgery, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Chao Xu
Lihua Sun
Min Yu
Ke Peng
Yuan Qiu
Weidong Xiao
Hua Yang
Army Medical University · CNXinqiao Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsThe pathogenesis of inflammatory bowel disease (IBD) is associated with dysregulation of intestinal immune system. Aryl hydrocarbon receptor (AHR) is believed to control the chronic inflammation in the gut. Besides, interleukin-7 (IL-7) is proved to be an important cytokine that activates mucosal inflammation in IBD. Moreover, intraepithelial lymphocytes (IELs) are one of the key immunological compartments involved in regulating intestinal inflammation. In this study, we investigated the function of 6-formylindolo (3,2-b) carbazole (Ficz), a ligand of AHR, on IL-7, colitis, and IEL phenotypes.

methodsColitis was induced by administration of dextran sulfate sodium (DSS) to wild-type C57BL/6J mice for 7 days. Mice were weighted, colon tissues were collected and measured, and histology analyses were performed. IELs were isolated from colon, and the phenotype and activation of IELs were examined using flow cytometry detection. The expression of AHR and IL-7 was measured by immunofluorescence, Western blot, and RT-PCR.

resultsFicz down-regulated epithelial-derived IL-7 expression in mice with DSS-induced colitis and ameliorated DSS-induced colitis. Ficz also decreased CD8αβ(+) and CD8(+) IEL subpopulations, enhanced TCRγδ(+) IEL subpopulation, and reduced the percentage of activated CD4(+) and CD8(+) subpopulations.

conclusionsFicz could down-regulate epithelial-derived IL-7 expression in mice with DSS-induced colitis and inhibit inflammation in the gastrointestinal tract of mice. AHR-related compounds might be the new and promising therapeutic medicaments for the treatment of patients with IBD.

Indexed as

AnimalsCarbazolesCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell LineColitisDextran SulfateGene Expression RegulationHumansInflammationInterleukin-7MiceReceptors, Aryl Hydrocarbon6-formylindolo(3,2-b)carbazoleCarbazolesDextran SulfateInterleukin-7Receptors, Aryl Hydrocarbon

Identifiers

PMID25799939
OpenAlexW2058907132

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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.