Evidence map›Paper›PMID 23925589›Full record

ArticleJournal of gastroenterology2014

Oral caffeine administration ameliorates acute colitis by suppressing chitinase 3-like 1 expression in intestinal epithelial cells.

In-Ah Lee, Daren Low, Alan Kamba, Victoria Llado, Emiko Mizoguchi

Open access · greenAbstract read
In one paragraph

Article in Journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
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  17. Beverage Consumption and Ulcerative Colitis: A Case-Control Study from Saudi Arabia.International journal of environmental research and public health · 2022
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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

5 authors at 2 institutions in 1 country.

In-Ah LeeGastrointestinal Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, GRJ 825D, 55 Fruit Street, Boston, MA, 02114, USA.
Daren Low
Alan Kamba
Victoria Llado
Emiko Mizoguchi
Massachusetts General Hospital · USHarvard University · US

Funding

Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI RAYMOND T CHUNG · 1991 to 2026
$35.3M
Xenograft and Isograft CoreP01DK033506 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI REINECKER, HANS-CHRISTIAN · 1986 to 2015
$24.2M
Antigen Recognition at Intestinal Epithelial InterphasesR01DK068181 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI REINECKER, HANS-CHRISTIAN · 2005 to 2017
$5.2M
Role of Mammalian Chitinases in Inflammatory Bowel DiseaseR01DK080070 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI MIZOGUCHI, EMIKO · 2009 to 2013
$1.6M
TNF Receptors of Colonic Epithelial Cells in IBDK08DK064289 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI MIZOGUCHI, EMIKO · 2003 to 2007
$637k
Mechanisms of Innate Immune Regulation for Mucosal HomeostasisR56AI093588 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI REINECKER, HANS-CHRISTIAN · 2011 to 2011
$362k
Regulatory Role of TNFR1 in Inflammatory Bowel DiseaseR03DK074454 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI MIZOGUCHI, EMIKO · 2006 to 2007
$172k
NIAID NIH HHS AI093588NIAID NIH HHS R56 AI093588NIDDK NIH HHS DK-033506NIDDK NIH HHS DK-068181NIDDK NIH HHS DK43351NIDDK NIH HHS DK64289NIDDK NIH HHS DK74454NIDDK NIH HHS DK 80070NIDDK NIH HHS K08 DK064289NIDDK NIH HHS P01 DK033506NIDDK NIH HHS P30 DK043351NIDDK NIH HHS R01 DK068181NIDDK NIH HHS R01 DK080070NIDDK NIH HHS R03 DK074454
6 · The paper itself

Abstract

backgroundThe initial trigger of inflammatory bowel disease (IBD) can be partly attributed towards the interaction and invasion of intestinal epithelial cells (IECs) and submucosal compartments. Identifying safe and economical methods to block these interactions may help prevent the onset of early colitis. Chitinase 3-like 1 (CHI3L1) is an inducible host protein that facilitates bacterial attachment and invasion on/into IECs. Therefore, we test the hypothesis of inhibiting CHI3L1 using the pan-chitinase inhibitor caffeine to reduce the likelihood of early colitis onset.

methodsIEC lines were treated with caffeine (2.5 or 5 mM) and analyzed for CHI3L1 expression and the impact on bacterial invasion. In vivo, mice were treated with 2.5 mM caffeine and induced with 3.5 % dextran sulfate sodium (DSS)-mediated colitis and subsequently analyzed colitis development.

resultsIn vitro, caffeine treatment in IEC lines down-regulated CHI3L1 mRNA expression, which resulted in the reduction of bacterial invasion in a caffeine dose-dependent manner. In vivo, mice treated with caffeine displayed a delayed response towards DSS-induced colitis, characterized by lower body weight loss, clinical and histological scores. Bacterial translocation into other organs and pro-inflammatory cytokines production were also reduced in the caffeine-treated mice with DSS-induced colitis. Caffeine treatment also resulted in the loss of CHI3L1-associated AKT signaling pathway activation both in vitro and in vivo.

conclusionDevelopment of acute colitis is reduced upon caffeine treatment. The mechanism involves the down-regulation of CHI3L1 expression and its associated bacterial interaction effect. Therefore, caffeine is proposed as a safe and economical candidate for successful IBD management.

Indexed as

Acute DiseaseAdipokinesAdministration, OralAnimalsBacterial TranslocationCaffeineCell LineChitinase-3-Like Protein 1ColitisDextran SulfateDisease Models, AnimalDose-Response Relationship, DrugDown-RegulationIntestinal MucosaLectinsMaleAdipokinesCaffeineCHI3L1 protein, humanChitinase-3-Like Protein 1Dextran SulfateLectinsRNA, Messenger

Identifiers

PMID23925589
PMCPMC3918252
OpenAlexW2076207814

What OpenQuestion holds

Textmetadata
LicenceTDM
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.