Evidence map›Paper›PMID 23691033›Full record

ArticlePloS one2013

Selective exposure of the fetal lung and skin/amnion (but not gastro-intestinal tract) to LPS elicits acute systemic inflammation in fetal sheep.

Matthew W Kemp, Paranthaman Senthamarai Kannan, Masatoshi Saito, John P Newnham, Tom Cox, Alan H Jobe, Boris W Kramer, Suhas G Kallapur

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.3field-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

21 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Innate immunity · 2020
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  6. Article
  7. Article
  8. Observational
  9. Intra-amniotic administration of lipopolysaccharide induces spontaneous preterm labor and birth in the absence of a body temperature change.The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2018
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  15. Article
  16. Article
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  18. Article
  19. Article
  20. Fetal immune response to chorioamnionitis.Seminars in reproductive medicine · 2014
    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

8 authors at 4 institutions in 4 countries.

Matthew W KempSchool of Women's and Infants' Health, The University of Western Australia, Perth, Australia.
Paranthaman Senthamarai Kannan
Masatoshi Saito
John P Newnham
Tom Cox
Alan H Jobe
Boris W Kramer
Suhas G Kallapur
University of Western Australia · AUCincinnati Children's Hospital Medical Center · USMaastricht University Medical Centre · NLTohoku University Hospital · JP

Funding

Mechanisms of Fetal Inflammatory Response Syndrome Induced by ChorioamnionitisR01HD057869 · NICHD · CINCINNATI CHILDRENS HOSP MED CTR · PI KALLAPUR, SUHAS · 2009 to 2013
$1.6M
NICHD NIH HHS HD 57869NICHD NIH HHS R01 HD057869
6 · The paper itself

Abstract

Inflammation of the uterine environment (commonly as a result of microbial colonisation of the fetal membranes, amniotic fluid and fetus) is strongly associated with preterm labour and birth. Both preterm birth and fetal inflammation are independently associated with elevated risks of subsequent short- and long-term respiratory, gastro-intestinal and neurological complications. Despite numerous clinical and experimental studies to investigate localised and systemic fetal inflammation following exposure to microbial agonists, there is minimal data to describe which fetal organ(s) drive systemic fetal inflammation. We used lipopolysaccharide (LPS) from E.coli in an instrumented ovine model of fetal inflammation and conducted a series of experiments to assess the systemic pro-inflammatory capacity of the three major fetal surfaces exposed to inflammatory mediators in pregnancy (the lung, gastro-intestinal tract and skin/amnion). Exposure of the fetal lung and fetal skin/amnion (but not gastro-intestinal tract) caused a significant acute systemic inflammatory response characterised by altered leucocytosis, neutrophilia, elevated plasma MCP-1 levels and inflammation of the fetal liver and spleen. These novel findings reveal differential fetal organ responses to pro-inflammatory stimulation and shed light on the pathogenesis of fetal systemic inflammation after exposure to chorioamnionitis.

Indexed as

AmnionAnalysis of VarianceAnimalsChemokine CCL2ChorioamnionitisEscherichia coliFemaleFetusLipopolysaccharidesLungPregnancySheepSheep DiseasesSystemic Inflammatory Response SyndromeChemokine CCL2Lipopolysaccharides

Identifiers

PMID23691033
PMCPMC3656923
OpenAlexW2051394900

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.