Evidence map›Paper›PMID 31917819›Full record

ArticlePloS one2020

Transgenic interleukin 11 expression causes cross-tissue fibro-inflammation and an inflammatory bowel phenotype in mice.

Wei-Wen Lim, Benjamin Ng, Anissa Widjaja, Chen Xie, Liping Su, Nicole Ko, Sze-Yun Lim, Xiu-Yi Kwek, Stella Lim, Stuart Alexander Cook and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing 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

40 citing papers in PubMed, 66 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. The role of IL-11 in chronic diseases.Frontiers in immunology · 2026
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  20. Selected Cytokines and Metalloproteinases in Inflammatory Bowel Disease.International journal of molecular sciences · 2023
    Review
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

11 authors at 2 institutions in 2 countries.

Wei-Wen LimNational Heart Research Institute Singapore, National Heart Centre Singapore, Singapore, Singapore.ORCID 0000-0003-0311-943X
Benjamin NgNational Heart Research Institute Singapore, National Heart Centre Singapore, Singapore, Singapore.
Anissa WidjajaCardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore, Singapore.ORCID 0000-0001-9404-7608
Chen XieNational Heart Research Institute Singapore, National Heart Centre Singapore, Singapore, Singapore.
Liping SuNational Heart Research Institute Singapore, National Heart Centre Singapore, Singapore, Singapore.
Nicole KoCardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore, Singapore.
Sze-Yun LimNational Heart Research Institute Singapore, National Heart Centre Singapore, Singapore, Singapore.
Xiu-Yi KwekNational Heart Research Institute Singapore, National Heart Centre Singapore, Singapore, Singapore.
Stella LimCardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore, Singapore.
Stuart Alexander CookNational Heart Research Institute Singapore, National Heart Centre Singapore, Singapore, Singapore.
Sebastian SchaferNational Heart Research Institute Singapore, National Heart Centre Singapore, Singapore, Singapore.
National University of Singapore · SGNational Heart Centre Singapore · SG

Funding

Medical Research Council MC_U120085815
6 · The paper itself

Abstract

Interleukin 11 (IL11) is a profibrotic cytokine, secreted by myofibroblasts and damaged epithelial cells. Smooth muscle cells (SMCs) also secrete IL11 under pathological conditions and express the IL11 receptor. Here we examined the effects of SMC-specific, conditional expression of murine IL11 in a transgenic mouse (Il11SMC). Within days of transgene activation, Il11SMC mice developed loose stools and progressive bleeding and rectal prolapse, which was associated with a 65% mortality by two weeks. The bowel of Il11SMC mice was inflamed, fibrotic and had a thickened wall, which was accompanied by activation of ERK and STAT3. In other organs, including the heart, lung, liver, kidney and skin there was a phenotypic spectrum of fibro-inflammation, together with consistent ERK activation. To investigate further the importance of stromal-derived IL11 in the inflammatory bowel phenotype we used a second model with fibroblast-specific expression of IL11, the Il11Fib mouse. This additional model largely phenocopied the Il11SMC bowel phenotype. These data show that IL11 secretion from the stromal niche is sufficient to drive inflammatory bowel disease in mice. Given that IL11 expression in colonic stromal cells predicts anti-TNF therapy failure in patients with ulcerative colitis or Crohn's disease, we suggest IL11 as a therapeutic target for inflammatory bowel disease.

Indexed as

PhenotypeAnimalsColonDisease ProgressionFibroblastsFibrosisGene ExpressionInflammatory Bowel DiseasesInterleukin-11MaleMiceMice, TransgenicMyocytes, Smooth MuscleInterleukin-11

Identifiers

PMID31917819
PMCPMC6952089
OpenAlexW2998926895

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.