Evidence map›Paper›PMID 32883198›Full record

ArticleMolecular medicine (Cambridge, Mass.)2020

Chorioamnionitis induces enteric nervous system injury: effects of timing and inflammation in the ovine fetus.

C Heymans, I H de Lange, K Lenaerts, L C G A Kessels, M Hadfoune, G Rademakers, V Melotte, W Boesmans, B W Kramer, A H Jobe and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
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  4. Next generation strategies for preventing preterm birth.Advanced drug delivery reviews · 2021
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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

14 authors at 5 institutions in 7 countries.

C HeymansDepartment of Surgery, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, the Netherlands.ORCID 0000-0001-9373-1360
I H de LangeDepartment of Surgery, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, the Netherlands.
K LenaertsDepartment of Surgery, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, the Netherlands.
L C G A KesselsDepartment of Pediatrics, School for Oncology and Developmental Biology (GROW), Maastricht University, P.O. Box 616, Universiteitssingel 50, 6200, MD, Maastricht, The Netherlands.
M HadfouneDepartment of Surgery, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, the Netherlands.
G RademakersDepartment of Pathology, School for Oncology and Developmental Biology (GROW), Maastricht University Medical Center, Maastricht, the Netherlands.
V MelotteDepartment of Pathology, School for Oncology and Developmental Biology (GROW), Maastricht University Medical Center, Maastricht, the Netherlands.
W BoesmansDepartment of Pathology, School for Oncology and Developmental Biology (GROW), Maastricht University Medical Center, Maastricht, the Netherlands.
B W KramerDepartment of Pediatrics, School for Oncology and Developmental Biology (GROW), Maastricht University, P.O. Box 616, Universiteitssingel 50, 6200, MD, Maastricht, The Netherlands.
A H JobeDivision of Obstetrics and Gynecology, The University of Western Australia, Crawley, Australia.
M SaitoDivision of Obstetrics and Gynecology, The University of Western Australia, Crawley, Australia.
M W KempDivision of Obstetrics and Gynecology, The University of Western Australia, Crawley, Australia.
W G van GemertDepartment of Surgery, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, the Netherlands.
T G A M WolfsDepartment of Pediatrics, School for Oncology and Developmental Biology (GROW), Maastricht University, P.O. Box 616, Universiteitssingel 50, 6200, MD, Maastricht, The Netherlands. tim.wolfs@maastrichtuniversity.nl.
Maastricht University · NLCincinnati Children's Hospital Medical Center · USMaastricht University Medical Centre · NLMurdoch University · AUThe University of Western Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChorioamnionitis, inflammation of the chorion and amnion, which often results from intrauterine infection, is associated with premature birth and contributes to significant neonatal morbidity and mortality, including necrotizing enterocolitis (NEC). Recently, we have shown that chronic chorioamnionitis is associated with significant structural enteric nervous system (ENS) abnormalities that may predispose to later NEC development. Understanding time point specific effects of an intra-amniotic (IA) infection on the ENS is important for further understanding the pathophysiological processes and for finding a window for optimal therapeutic strategies for an individual patient. The aim of this study was therefore to gain insight in the longitudinal effects of intrauterine LPS exposure (ranging from 5 h to 15 days before premature delivery) on the intestinal mucosa, submucosa, and ENS in fetal lambs by use of a well-established translational ovine chorioamnionitis model.

methodsWe used an ovine chorioamnionitis model to assess outcomes of the fetal ileal mucosa, submucosa and ENS following IA exposure to one dose of 10 mg LPS for 5, 12 or 24 h or 2, 4, 8 or 15 days.

resultsFour days of IA LPS exposure causes a decreased PGP9.5- and S100β-positive surface area in the myenteric plexus along with submucosal and mucosal intestinal inflammation that coincided with systemic inflammation. These changes were preceded by a glial cell reaction with early systemic and local gut inflammation. ENS changes and inflammation recovered 15 days after the IA LPS exposure.

conclusionsThe pattern of mucosal and submucosal inflammation, and ENS alterations in the fetus changed over time following IA LPS exposure. Although ENS damage seemed to recover after prolonged IA LPS exposure, additional postnatal inflammatory exposure, which a premature is likely to encounter, may further harm the ENS and influence functional outcome. In this context, 4 to 8 days of IA LPS exposure may form a period of increased ENS vulnerability and a potential window for optimal therapeutic strategies.

Indexed as

AnimalsAutonomic Nervous System DiseasesBiomarkersChorioamnionitisDisease Models, AnimalEnteric Nervous SystemEnterocolitis, NecrotizingFemaleIntestinal MucosaPregnancyPremature BirthSheepSheep DiseasesBiomarkersChorioamnionitisEnteric nervous systemIntra-amniotic infectionLPSNecrotizing enterocolitisPreterm birthSheep

Identifiers

PMID32883198
PMCPMC7469100
OpenAlexW3083025947

What OpenQuestion holds

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LicenceCC BY
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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.