Evidence map›Paper›PMID 28753596›Full record

ArticlePediatric research2017

Inhibition of IκBβ/NFκB signaling prevents LPS-induced IL1β expression without increasing apoptosis in the developing mouse lung.

Sarah McKenna, Brittany Butler, Laurie Jatana, Sankar Ghosh, Clyde J Wright

Open access · bronzeAbstract read
In one paragraph

Article in Pediatric research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.8field-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

16 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Lung organoids: a new frontier in neonatology and paediatric respiratory medicine.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
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  14. MyeloidJournal of immunology (Baltimore, Md. : 1950) · 2019
    Article
  15. Article
  16. Article
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.

Sarah McKennaSection of Neonatology, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado.
Brittany ButlerSection of Neonatology, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado.
Laurie JatanaSection of Neonatology, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado.
Sankar GhoshDepartment of Microbiology & Immunology, College of Physicians and Surgeons, Columbia University, New York, New York.
Clyde J WrightSection of Neonatology, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado.
University of Colorado Denver · USColumbia University · US

Funding

Role of hepatic IkBb-mediated sustained NFkB activation in neonatal lung injury and abnormal developmentR01HL132941 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI WRIGHT, CLYDE JASON · 2017 to 2021
$2.3M
The unique role of IkBa in modulating NF-kB activity in the newborn lung.K08HL098562 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI WRIGHT, CLYDE JASON · 2010 to 2014
$670k
NHLBI NIH HHS K08 HL098562NHLBI NIH HHS R01 HL132941
6 · The paper itself

Abstract

BackgroundThe pro-inflammatory consequences of IL1β expression contribute to the pathogenesis of bronchopulmonary dysplasia. Selectively targeting Lipopolysaccharide (LPS)-induced IκBβ/NFκB signaling attenuates IL1β mRNA expression in macrophages. Whether targeting IκBβ/NFκB signaling affects the anti-apoptotic gene expression, a known consequence of global LPS-induced NFκB inhibition, is unknown.MethodsMacrophages (RAW 264.7, bone marrow-derived macrophage) were assessed for LPS-induced IL1β mRNA/protein expression, anti-apoptotic gene expression, cell viability (trypan blue exclusion), and activation of apoptosis (caspase-3 and PARP cleavage) following pharmacologic and genetic attenuation of IκBβ/NFκB signaling. Expressions of IL1β and anti-apoptotic genes were assessed in endotoxemic newborn mice (P0) with intact (WT), absent (IκBβ KO), and attenuated (IκBβ overexpressing) IκBβ/NFκB signaling.ResultsIn cultured macrophages, pharmacologic and genetic inhibition of LPS-induced IκBβ/NFκB signaling significantly attenuated IL1β mRNA and protein expression. Importantly, targeting IκBβ/NFκB signaling did not attenuate LPS-induced expression of anti-apoptotic genes or result in cell death. In endotoxemic neonatal mice, targeting LPS-induced IκBβ/NFκB signaling significantly attenuated pulmonary IL1β expression without affecting the anti-apoptotic gene expression.ConclusionTargeting IκBβ/NFκB signaling prevents LPS-induced IL1β expression without inducing apoptosis in cultured macrophages and in the lungs of endotoxemic newborn mice. Inhibiting this pathway may prevent inflammatory injury without affecting the protective role of NFκB activity in the developing lung.

Indexed as

AnimalsAnimals, NewbornApoptosisCell LineI-kappa B ProteinsInterleukin-1betaLipopolysaccharidesLungMacrophagesMiceMice, Inbred ICRNF-kappa BRNA, MessengerSignal TransductionI kappa B beta proteinI-kappa B ProteinsInterleukin-1betaLipopolysaccharidesNF-kappa BRNA, Messenger

Identifiers

PMID28753596
PMCPMC5761659
OpenAlexW2740070809

What OpenQuestion holds

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Registered trials

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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.