Evidence map›Paper›PMID 24301657›Full record

ArticleMucosal immunology2014

IL-10 modulates DSS-induced colitis through a macrophage-ROS-NO axis.

B Li, R Alli, P Vogel, T L Geiger

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 5% 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

108 citing papers in PubMed, 1 synthesis or guideline pooled it, 182 citations in OpenAlex.

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  13. CNPY2 drives DSS-induced colitis via the macrophage-ROS axis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
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48 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

B LiDepartment of Pathology, St Jude Children's Research Hospital, Memphis, Tennessee, USA.
R AlliDepartment of Pathology, St Jude Children's Research Hospital, Memphis, Tennessee, USA.
P VogelDepartment of Pathology, St Jude Children's Research Hospital, Memphis, Tennessee, USA.
T L GeigerDepartment of Pathology, St Jude Children's Research Hospital, Memphis, Tennessee, USA.
St. Jude Children's Research Hospital · US

Funding

TREATMENT OF AUTOIMMUNITY WITH REGULATORY T LYMPHOCYTESR01AI056153 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI GEIGER, TERRENCE L · 2004 to 2013
$3.9M
Lineage Specific Effects of IL10 In AutoimmunityR56AI106600 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI GEIGER, TERRENCE L · 2013 to 2013
$411k
NIAID NIH HHS R01 AI056153NIAID NIH HHS R01AI056153NIAID NIH HHS R56 AI006600NIAID NIH HHS R56 AI106600
6 · The paper itself

Abstract

Breakdown of the epithelial barrier because of toxins or other insults leads to severe colitis. Interleukin-10 (IL-10) is a critical regulator of this, yet its cellular targets and mechanisms of action are not resolved. We address this here. Mice with a macrophage-selective deletion of IL-10Rα (IL-10Rα(Mdel)) developed markedly enhanced dextran sodium sulfate (DSS)-induced colitis that did not significantly differ from disease in IL-10(-/-) or IL-10Rα(-/-) mice; no impact of IL-10Rα deficiency in other lineages was observed. IL-10Rα(Mdel) colitis was associated with increased mucosal barrier disruption in the setting of intact epithelial regeneration. Lamina propria macrophages (LPMφs) did not show numerical or phenotypic differences from controls, or a competitive advantage over wild-type cells. Proinflammatory cytokine production, and particularly tumor necrosis factor-α (TNF-α), was increased, although TNF-α neutralization failed to reveal a defining role for this cytokine in the aggravated disease. Rather, IL-10Rα(Mdel) LPMφs produced substantially greater levels of nitric oxide (NO) and reactive oxygen species (ROS) than controls. Inhibition of these had modest effects in wild-type mice, although they dramatically reduced colitis severity in IL-10Rα(Mdel) mice, and largely eliminated the differential effect of DSS in them. Therefore, the palliative actions of IL-10 in DSS-induced colitis predominantly results from its macrophage-specific effects. Downregulation of NO and ROS production are central to the protective actions of IL-10.

Indexed as

AnimalsColitisCytokinesDextran SulfateDisease Models, AnimalGene ExpressionInflammation MediatorsInterleukin-10Interleukin-10 Receptor alpha SubunitIntestinal MucosaMacrophagesMiceMice, KnockoutNitric OxideReactive Oxygen SpeciesCytokinesDextran SulfateInflammation MediatorsInterleukin-10Interleukin-10 Receptor alpha SubunitNitric OxideReactive Oxygen Species

Identifiers

PMID24301657
PMCPMC4045662
OpenAlexW2011093795

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.