Evidence map›Paper›PMID 32662549›Full record

ArticleAmerican journal of reproductive immunology (New York, N.Y. : 1989)2020

The role of in utero endotoxin exposure in the development of inflammatory bowel disease in mice.

Emilyn Banfield, William Fulton, Irina Burd, Mark L Kovler, Chhinder P Sodhi, David J Hackam

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of reproductive immunology (New York, N.Y. : 1989), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

6 authors.

Emilyn BanfieldDepartment of Human Genetics, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
William FultonDivision of Pediatric Surgery, Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Irina BurdDivision of Maternal Fetal Medicine, Department of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Mark L KovlerDivision of Pediatric Surgery, Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Chhinder P SodhiDivision of Pediatric Surgery, Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
David J HackamDepartment of Human Genetics, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0001-5195-8807

Funding

Predoctoral Training Program in Human GeneticsT32GM007814 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI VALLE, DAVID · 1985 to 2021
$10.6M
TLR4 Signaling in the Pathogenesis of Surgical Necrotizing EnterocolitisR01GM078238 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HACKAM, DAVID J · 2006 to 2019
$3.9M
Modulation of TLR4 and TLR9 Signaling in NECR01DK083752 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HACKAM, DAVID J · 2008 to 2016
$3.4M
Maternal-Fetal AHR Signaling in the Pathogenesis and Treatment of Necrotizing EnterocolitisR01DK117186 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI HACKAM, DAVID J · 2018 to 2021
$1.5M
Enteric Glia Regulation of Intestinal Epithelial TLR4 Signaling In Necrotizing EnterocolitisR01DK121824 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI HACKAM, DAVID J · 2020 to 2023
$1.4M
NIDDK NIH HHS R01 DK083752NIDDK NIH HHS R01 DK117186NIDDK NIH HHS R01 DK121824NIGMS NIH HHS R01 GM078238NIGMS NIH HHS T32 GM007814
6 · The paper itself

Abstract

problemAlthough early environmental influences are thought to influence the development of inflammatory bowel disease (IBD), little is known about the role of the in utero environment on subsequent IBD risk. We hypothesized that prenatal exposure to bacterial lipopolysaccharide (LPS) could modify the subsequent development of dextran sulfate sodium (DSS)-induced ulcerative colitis in adulthood by influencing the associated cellular and immune response. METHOD OF STUDY: To test this hypothesis, we exposed developing mice in utero to LPS or saline (PBS) at E17.5, and then induced colitis at 5 weeks. We then assessed colitis severity and effects on the microbiome. In order to define the developmental impact of any potential LPS effect, we also exposed 1-week-old mice to either LPS or saline before inducing colitis at 5 weeks.

resultsMice that had been exposed to LPS but not saline in utero were protected from subsequent colitis development, and their intestinal barrier integrity and tight junction expression distribution were similar to that of control mice that were not exposed to DSS. By contrast, mice exposed to either LPS or saline at day 7 of life all developed severe colitis upon subsequent DSS exposure.

conclusionThese results identify an informative time window during fetal development during which exposure to an otherwise pro-inflammatory agent like LPS protects against an inflammatory disease in adulthood.

Indexed as

AnimalsColitis, UlcerativeDextran SulfateDisease Models, AnimalDisease ResistanceFemaleGastrointestinal MicrobiomeHumansImmunity, CellularInflammatory Bowel DiseasesLipopolysaccharidesMiceMice, Inbred C57BLPregnancyPrenatal Exposure Delayed EffectsUterusDextran SulfateLipopolysaccharidesfetal developmentinflammatory bowel diseaselipopolysaccharide

Identifiers

PMID32662549
PMCPMC7722031

What OpenQuestion holds

Textmetadata
LicenceTDM
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.