Evidence map›Paper›PMID 28490020›Full record

ArticleDevelopmental neuroscience2017

Maternal Inflammation Results in Altered Tryptophan Metabolism in Rabbit Placenta and Fetal Brain.

Monica Williams, Zhi Zhang, Elizabeth Nance, Julia L Drewes, Wojciech G Lesniak, Sarabdeep Singh, Diane C Chugani, Kannan Rangaramanujam, David R Graham, Sujatha Kannan

Open access · bronzeAbstract read
In one paragraph

Article in Developmental neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 62 citations in OpenAlex.

  1. Gestational kynurenine metabolites mediate effects of pregnancy adiposity on child negative affect.Journal of child psychology and psychiatry, and allied disciplines · 2026
    Article
  2. Review
  3. Modeling cerebral palsy in animals.Developmental medicine and child neurology · 2026
    Review
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  14. Proposed Pathway Linking Respiratory Infections with Depression.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2022
    Review
  15. Article
  16. Review
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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

10 authors at 2 institutions in 1 country.

Monica WilliamsDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University SOM, Baltimore, MD, USA.
Zhi Zhang
Elizabeth Nance
Julia L Drewes
Wojciech G Lesniak
Sarabdeep Singh
Diane C Chugani
Kannan Rangaramanujam
David R Graham
Sujatha Kannan
Johns Hopkins University · USCommunity Health Systems - Dupont Hospital · US

Funding

Program in Postdoctoral Research Training in AnesthesiologyT32GM075774 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI SAPNA R KUDCHADKAR, Emmett E Whitaker · 2006 to 2026
$8.1M
Mechanisms and novel therapy in intrauterine inflammation induced brain injuryR01HD069562 · NICHD · JOHNS HOPKINS UNIVERSITY · PI KANNAN, SUJATHA · 2012 to 2016
$1.6M
NICHD NIH HHS R01 HD069562NIGMS NIH HHS T32 GM075774
6 · The paper itself

Abstract

Maternal inflammation has been linked to neurodevelopmental and neuropsychiatric disorders such as cerebral palsy, schizophrenia, and autism. We had previously shown that intrauterine inflammation resulted in a decrease in serotonin, one of the tryptophan metabolites, and a decrease in serotonin fibers in the sensory cortex of newborns in a rabbit model of cerebral palsy. In this study, we hypothesized that maternal inflammation results in alterations in tryptophan pathway enzymes and metabolites in the placenta and fetal brain. We found that intrauterine endotoxin administration at gestational day 28 (G28) resulted in a significant upregulation of indoleamine 2,3-dioxygenase (IDO) in both the placenta and fetal brain at G29 (24 h after treatment). This endotoxin-mediated IDO induction was also associated with intense microglial activation, an increase in interferon gamma expression, and increases in kynurenine and the kynurenine pathway metabolites kynurenine acid and quinolinic acid, as well as a significant decrease in 5-hydroxyindole acetic acid (a precursor of serotonin) levels in the periventricular region of the fetal brain. These results indicate that maternal inflammation shunts tryptophan metabolism away from the serotonin to the kynurenine pathway, which may lead to excitotoxic injury along with impaired development of serotonin-mediated thalamocortical fibers in the newborn brain. These findings provide new targets for prevention and treatment of maternal inflammation-induced fetal and neonatal brain injury leading to neurodevelopmental disorders such as cerebral palsy and autism.

Indexed as

AnimalsBrainFemaleIndolesInflammationPlacentaPregnancyQuinolinic AcidRabbitsSerotoninTryptophan5-hydroxyindoleIndolesQuinolinic AcidSerotoninTryptophanAutismCerebral palsyKynurenine pathwayMaternal infectionMicrogliaSerotoninTryptophan

Identifiers

PMID28490020
PMCPMC6447288
OpenAlexW2613065894

What OpenQuestion holds

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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.