Evidence map›Paper›PMID 20923949›Full record

ArticleReproductive sciences (Thousand Oaks, Calif.)2011

Exposure to in utero lipopolysaccharide induces inflammation in the fetal ovine skin.

Matthew W Kemp, Masatoshi Saito, Ilias Nitsos, Alan H Jobe, Suhas G Kallapur, John P Newnham

Abstract read
In one paragraph

Article in Reproductive sciences (Thousand Oaks, Calif.), 2011. 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
3.2field-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

27 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Innate immunity · 2020
    Article
  4. Article
  5. 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
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Sterile and microbial-associated intra-amniotic inflammation in preterm prelabor rupture of membranes.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 · 2015
    Article
  11. Article
  12. Article
  13. The diagnostic performance of the Mass Restricted (MR) score in the identification of microbial invasion of the amniotic cavity or intra-amniotic inflammation is not superior to amniotic fluid interleukin-6.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 · 2014
    Article
  14. Article
  15. Fetal immune response to chorioamnionitis.Seminars in reproductive medicine · 2014
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 1 institution in 3 countries.

Matthew W KempSchool of Women's and Infants' Health, The University of Western Australia, Perth, Australia. mkemp@meddent.uwa.edu.au
Masatoshi Saito
Ilias Nitsos
Alan H Jobe
Suhas G Kallapur
John P Newnham
University of Western Australia · AU

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 is a defensive process by which the body responds to both localized and systemic tissue damage by the induction of innate and adaptive immunity. Literature from human and animal studies links inappropriate in utero inflammation to preterm parturition and fetal injury. The pathways by which such inflammation may cause labor, however, are not fully understood. Any proinflammatory agonist in the amniotic fluid will contact the fetal skin, in its entirety, but a potential role of the fetal skin in the pathways to labor have not previously been explored. We hypothesized that the fetal skin would respond robustly to the presence of intra-amniotic lipopolysaccharide (LPS) in our ovine model of in utero inflammation. In vitro and in utero exposure of fetal ovine keratinocytes or fetal skin to Escherichia coli LPS reliably induced significant increases in interleukin 1β (IL-1β), IL-6, tumor necrosis factor α (TNF-α), and IL-8 expression. We demonstrate that, in utero, this expression requires direct exposure with LPS suggesting that the inflammation is triggered directly in the skin itself, rather than as a secondary response to a systemic stimuli and that inflammation involves Toll-like receptor (TLR) regulation and neutrophil chemotaxis in concordance with an acute inflammatory reaction. We show that this response involves multiple inflammatory mediators, TLR regulation, and localized inflammatory cell influx characteristic of an acute inflammatory reaction. These novel data strongly suggests that the fetal skin acts as an important mediator of the fetal inflammatory response and as such may contribute to preterm birth.

Indexed as

AmnionAnimalsCells, CulturedDermatitis, ContactEscherichia coliFemaleFetal DiseasesGene ExpressionImmunohistochemistryInterleukin-1Interleukin-1betaInterleukin-8KeratinocytesLipopolysaccharidesPolymerase Chain ReactionPregnancyInterleukin-1Interleukin-1betaInterleukin-8LipopolysaccharidesRNA, MessengerToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID20923949
PMCPMC3343071
OpenAlexW2096596174

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.