Evidence map›Paper›PMID 25105257›Full record

ArticlePediatric research2014

Intra-amniotic LPS modulates expression of antimicrobial peptides in the fetal sheep lung.

Augusto F Schmidt, Paranthaman S Kannan, Matthew W Kemp, Boris W Kramer, John P Newnham, Alan H Jobe, Suhas G Kallapur

Open access · bronzeAbstract read
In one paragraph

Article in Pediatric research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

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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

7 authors at 3 institutions in 3 countries.

Augusto F SchmidtDivision of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio.
Paranthaman S KannanDivision of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio.ORCID 0000000233333720
Matthew W KempSchool of Women's and Infants' Health, The University of Western Australia, Perth, Australia.
Boris W KramerDepartment of Pediatrics, Maastricht University Medical Center, Maastricht, The Netherlands.
John P NewnhamSchool of Women's and Infants' Health, The University of Western Australia, Perth, Australia.
Alan H JobeDivision of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio.
Suhas G KallapurDivision of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio.
Cincinnati Children's Hospital Medical Center · USThe University of Western Australia · AUMaastricht University · NL

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

backgroundDamage-associated molecular patterns (DAMPs) and antimicrobial peptides (AMPs) are components of pulmonary innate immunity and tissue repair. We hypothesized that DAMPs and AMPs would increase in response to fetal pulmonary inflammation caused by chorioamnionitis in a time-dependent manner.

methodsFetal sheep were exposed to intra-amniotic saline or lipopolysaccharide (LPS) (10 mg) between 5 h and 15 d prior to preterm delivery at 125 ± 2 d. Lung tissue mRNAs for proinflammatory cytokines; AMPs: myeloid AMP-29 (MAP29), dodecapeptide, sheep β-defensin-1 (SBD1), and sheep β-defensin-2 (SBD2); and DAMPs: interleukin (IL)-1α, lactoferrin, heat-shock protein-70 (HSP70), high-mobility group box protein-B1 (HMGB1), and receptor for advanced glycation endproducts (RAGE) were measured by reverse-transcriptase quantitative polymerase chain reaction. Immunohistochemistry of DAMPs and in situ hybridization of AMPs was performed.

resultsIL-1α, IL-1β, IL-6, IL-8, IL-10, MCP-1, and tumor necrosis factor (TNF)-α mRNA increased after LPS exposure. MAP29, dodecapeptide, SBD1, and SBD2 mRNA were suppressed at 24 h. MAP29 and dodecapeptide mRNA then increased at 8 d. Lactoferrin increased at 24 h. There were no changes for HMGB1, HSP70, or RAGE. MAP29 and dodecapeptide localized to alveolar cells, increased 8 d after exposure to LPS.

conclusionAMPs are initially suppressed in the fetal lung by LPS-induced chorioamnionitis. The late induction of MAP29 and dodecapeptide may be related to lung repair.

Indexed as

LipopolysaccharidesAmniotic FluidAnimalsAntimicrobial Cationic PeptidesChorioamnionitisCytokinesDisease Models, AnimalFemaleGene Expression RegulationGestational AgeInflammation MediatorsLungPregnancyPremature BirthRNA, MessengerSheepAntimicrobial Cationic PeptidesCytokinesInflammation MediatorsLipopolysaccharidesRNA, Messenger

Identifiers

PMID25105257
PMCPMC4213214
OpenAlexW2025997018

What OpenQuestion holds

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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.