Evidence map›Paper›PMID 24992040›Full record

ArticlePloS one2014

The role of CXCR3 in DSS-induced colitis.

Belal Chami, Amanda W S Yeung, Caryn van Vreden, Nicholas J C King, Shisan Bao

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 62 citations in OpenAlex.

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  16. Effects of Aqueous and Methanolic Extracts of Stem Bark ofEvidence-based complementary and alternative medicine : eCAM · 2020
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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 3 institutions in 1 country.

Belal ChamiDiscipline of Pathology, Bosch Institute and School of Medical Sciences, Sydney Medical School, The University of Sydney, Sydney, NSW, Australia.
Amanda W S YeungCentre for Vascular Research, Lowy Cancer Research Centre, University of New South Wales, Sydney, NSW, Australia.
Caryn van VredenDiscipline of Pathology, Bosch Institute and School of Medical Sciences, Sydney Medical School, The University of Sydney, Sydney, NSW, Australia.
Nicholas J C KingDiscipline of Pathology, Bosch Institute and School of Medical Sciences, Sydney Medical School, The University of Sydney, Sydney, NSW, Australia; Sydney Institute of Emerging infectious diseases and Biosecurity (SEIB), Sydney Medical School, University of Sydney, Sydney, NSW, Australia.
Shisan BaoDiscipline of Pathology, Bosch Institute and School of Medical Sciences, Sydney Medical School, The University of Sydney, Sydney, NSW, Australia.
University of Sydney · AUTaronga Conservation Society Australia · AUUNSW Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory bowel disease (IBD) is a group of disorders that are characterized by chronic, uncontrolled inflammation in the intestinal mucosa. Although the aetiopathogenesis is poorly understood, it is widely believed that IBD stems from a dysregulated immune response towards otherwise harmless commensal bacteria. Chemokines induce and enhance inflammation through their involvement in cellular trafficking. Reducing or limiting the influx of these proinflammatory cells has previously been demonstrated to attenuate inflammation. CXCR3, a chemokine receptor in the CXC family that binds to CXCL9, CXCL10 and CXCL11, is strongly overexpressed in the intestinal mucosa of IBD patients. We hypothesised that CXCR3 KO mice would have impaired cellular trafficking, thereby reducing the inflammatory insult by proinflammatory cell and attenuating the course of colitis. To investigate the role of CXCR3 in the progression of colitis, the development of dextran sulfate sodium (DSS)-induced colitis was investigated in CXCR3-/- mice over 9 days. This study demonstrated attenuated DSS-induced colitis in CXCR3-/- mice at both the macroscopic and microscopic level. Reduced colitis correlated with lower recruitment of neutrophils (p = 0.0018), as well as decreased production of IL-6 (p<0.0001), TNF (p = 0.0038), and IFN-γ (p = 0.0478). Overall, our results suggest that CXCR3 plays an important role in recruiting proinflammatory cells to the colon during colitis and that CXCR3 may be a therapeutic target to reduce the influx of proinflammatory cells in the inflamed colon.

Indexed as

ColitisInflammatory Bowel DiseasesIntestinal MucosaAnimalsCytokinesDextran SulfateMiceMice, KnockoutReceptors, CXCR3Cxcr3 protein, mouseCytokinesDextran SulfateReceptors, CXCR3

Identifiers

PMID24992040
PMCPMC4081590
OpenAlexW1978820698

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.