Evidence map›Paper›PMID 28846670›Full record

ArticlePediatric research2018

Single-Immunoglobulin Interleukin-1-Related Receptor regulates vulnerability to TLR4-mediated necrotizing enterocolitis in a mouse model.

Jason Fawley, Alain Cuna, Heather L Menden, Steven McElroy, Shahid Umar, Scott R Welak, David M Gourlay, Xiaoxia Li, Venkatesh Sampath

Open access · bronzeAbstract read
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In one paragraph

Article in Pediatric research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

27 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  8. The Role of the Interleukin-1 Family in Complications of Prematurity.International journal of molecular sciences · 2023
    Review
  9. Article
  10. State-of-the-art review and update ofFrontiers in pediatrics · 2023
    Review
  11. Article
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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 5 institutions in 1 country.

Jason FawleyDepartment of Pediatric Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin.
Alain CunaDepartment of Pediatrics, Children's Mercy Hospital, Kansas City, Missouri.
Heather L MendenDepartment of Pediatrics, Children's Mercy Hospital, Kansas City, Missouri.
Steven McElroyStead Family Department of Pediatrics, University of Iowa, Iowa City, Iowa.
Shahid UmarDepartment of Surgery, Kansas University Medical Center, Kansas City, Missouri.
Scott R WelakDepartment of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin.
David M GourlayDepartment of Pediatric Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin.
Xiaoxia LiDepartment of Molecular Medicine, Cleveland Clinic Lerner Research Institute, Cleveland, Ohio.
Venkatesh SampathDepartment of Pediatrics, Children's Mercy Hospital, Kansas City, Missouri.
Children's Mercy Hospital · USMedical College of Wisconsin · USCleveland Clinic Lerner College of Medicine · USUniversity Medical Center · USUniversity of Iowa · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BackgroundThe mechanisms underlying aberrant activation of intestinal Toll-like receptor 4 (TLR4) signaling in necrotizing enterocolitis (NEC) remain unclear. In this study, we examined the role of single-immunoglobulin interleukin-1 receptor-related molecule (SIGIRR), an inhibitor of TLR signaling, in modulating experimental NEC vulnerability in mice.MethodsExperimental NEC was induced in neonatal wild-type and SIGIRR-/- mice using hypoxia, formula-feeding, and lipopolysaccharide administration. Intestinal TLR canonical signaling, inflammation, apoptosis, and severity of experimental NEC were examined at baseline and after NEC induction in mice.ResultsSIGIRR is developmentally regulated in the neonatal intestine with a restricted expression after birth and a gradual increase by day 8. At baseline, breast-fed SIGIRR-/- mouse pups exhibited low-grade inflammation and TLR pathway activation compared with SIGIRR+/+ pups. With experimental NEC, SIGIRR-/- mice had significantly more intestinal interleukin (IL)-1β, KC (mouse homolog to IL-8), intercellular adhesion molecule-1 (ICAM-1), and interferon-beta (IFN-β) expression in association with the amplified TLR pathway activation. Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining, cleaved caspase 3, and severity of intestinal injury with NEC were worse in SIGIRR-/- mice in comparison with SIGIRR+/+ mice.ConclusionSIGIRR is a negative regulator of TLR4 signaling in the developing intestine, and its insufficiency results in native intestinal TLR hyper-responsiveness conducive to the development of severe experimental NEC in mice.

Indexed as

AnimalsAnimals, NewbornApoptosisCytokinesDisease Models, AnimalEnterocolitis, NecrotizingHypoxiaImmunity, InnateInflammationLipopolysaccharidesMiceMice, Inbred C57BLMice, TransgenicMutationPhosphorylationReceptors, Interleukin-1CytokinesLipopolysaccharidesReceptors, Interleukin-1SIGIRR protein, mouseTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID28846670
OpenAlexW2748989199

What OpenQuestion holds

Textmetadata
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.