Evidence map›Paper›PMID 24694795›Full record

ArticleInflammatory bowel diseases2014

Chitinase 3-like 1 synergistically activates IL6-mediated STAT3 phosphorylation in intestinal epithelial cells in murine models of infectious colitis.

Hoa T Tran, In-Ah Lee, Daren Low, Alan Kamba, Atsushi Mizoguchi, Hai N Shi, Chun G Lee, Jack A Elias, Emiko Mizoguchi

Open access · bronzeAbstract read
In one paragraph

Article in Inflammatory bowel diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

26 citing papers in PubMed, 80 citations in OpenAlex.

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  12. Potential role of chitinase-3-like protein 1 (CHI3L1/YKL-40) in neurodegeneration and Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    Article
  13. Review
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  17. Chitinase-3 like-protein-1 function and its role in diseases.Signal transduction and targeted therapy · 2020
    Review
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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

9 authors at 4 institutions in 3 countries.

Hoa T Tran*Gastrointestinal Unit and †Center for the Study of Inflammatory Bowel Disease, Department of Medicine, ‡Molecular Pathology Unit, Department of Pathology, and §Division of Mucosal Immunology, Department of Pediatrics, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts; and ‖Section of Pulmonary and Critical Care Medicine, Department of Medicine, Yale University School of Medicine, New Haven, Connecticut.
In-Ah Lee
Daren Low
Alan Kamba
Atsushi Mizoguchi
Hai N Shi
Chun G Lee
Jack A Elias
Emiko Mizoguchi
German Inflammatory Bowel Diseases Study Group · DEInstitute of Molecular Medicine · INMassachusetts General Hospital · USYale University · US

Funding

Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI RAYMOND T CHUNG · 1991 to 2026
$35.3M
YKL-40 in Idiopathic Pulmonary Fibrosis and Kidney TransplantationU01HL108638 · NHLBI · YALE UNIVERSITY · PI ELIAS, JACK A · 2011 to 2014
$2.6M
Role of Mammalian Chitinases in Inflammatory Bowel DiseaseR01DK080070 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI MIZOGUCHI, EMIKO · 2009 to 2013
$1.6M
NHLBI NIH HHS U01 HL108638NIDDK NIH HHS P30 DK043351NIDDK NIH HHS R01 DK080070NIDDK NIH HHS R01-DK80070
6 · The paper itself

Abstract

backgroundChitinase 3-like 1 (CHI3L1) is an inducible molecule on intestinal epithelial cells during the development of inflammatory bowel disease.

methodsTo investigate the role of CHI3L1 in bacterial infectious colitis, we orally inoculated pathogenic Salmonella typhimurium and potentially pathogenic adherent-invasive Escherichia coli (AIEC) LF82 virulent strain into C57Bl/6 wild-type mice or CHI3L1 knockout (KO) mice.

resultsBoth S. typhimurium and AIEC LF82 were found to efficiently induce severe intestinal inflammation in wild-type mice but not in CHI3L1 KO mice. These bacteria-infected CHI3L1 KO mice exhibit decreased cellular infiltration, bacterial translocation, and production of interleukin (IL)-6 and IL-22, as compared with those of wild-type mice. More importantly, CHI3L1 KO mice displayed aberrant STAT3 activation after bacterial infections. Co-stimulation of CHI3L1 and IL-6, but not IL-22, synergistically activates STAT3 signaling pathway in intestinal epithelial cells in an NF-κB/MAPK-dependent manner.

conclusionsCHI3L1 promotes the onset of selected gram-negative bacterial infectious colitis through IL-6/STAT3 pathway.

Indexed as

Disease Models, AnimalAnimalsBacterial AdhesionBlotting, WesternCells, CulturedChitinase-3-Like Protein 1ColitisEpithelial CellsEscherichia coliEscherichia coli InfectionsGlycoproteinsImmunoenzyme TechniquesInterleukin-6Intestinal MucosaMiceMice, Inbred C57BLChil1 protein, mouseChitinase-3-Like Protein 1GlycoproteinsInterleukin-6NF-kappa BStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID24694795
PMCPMC4012618
OpenAlexW2017013500

What OpenQuestion holds

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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.