Evidence map›Paper›PMID 30267854›Full record

ArticleProgress in neuro-psychopharmacology & biological psychiatry2019

Maternal immune activation in rats blunts brain cytokine and kynurenine pathway responses to a second immune challenge in early adulthood.

Sarah M Clark, Francesca M Notarangelo, Xin Li, Shuo Chen, Robert Schwarcz, Leonardo H Tonelli

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Article in Progress in neuro-psychopharmacology & biological psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 52 citations in OpenAlex.

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  10. Animal Models of Relevance to the Schizophrenia Prodrome.Biological psychiatry global open science · 2023
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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

6 authors at 1 institution in 1 country.

Sarah M ClarkLaboratory of Behavioral Neuroimmunology, Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, USA.
Francesca M NotarangeloMaryland Psychiatric Research Center, Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, USA.
Xin LiLaboratory of Behavioral Neuroimmunology, Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, USA.
Shuo ChenMaryland Psychiatric Research Center, Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, USA.
Robert SchwarczMaryland Psychiatric Research Center, Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, USA.
Leonardo H TonelliLaboratory of Behavioral Neuroimmunology, Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, USA. Electronic address: ltonelli@som.umaryland.edu.
University of Maryland, Baltimore · US

Funding

The Effects of Kynurenine Aminotransferase Inhibition in People with SchizophreniaP50MH103222 · NIMH · UNIVERSITY OF MARYLAND BALTIMORE · PI SCHWARCZ, ROBERT · 2014 to 2023
$25.2M
NIMH NIH HHS P50 MH103222
6 · The paper itself

Abstract

Maternal immune activation (MIA) with the viral mimic poly I:C provides an established rodent model for studying schizophrenia (SZ) and other human neurodevelopmental disorders. Postnatal infections are additional risk factors in SZ and may cumulatively contribute to the emergence of pathophysiology. Underlying mechanisms may involve metabolites of the kynurenine pathway (KP) of tryptophan degradation, which is readily induced by inflammatory stimuli. Here we compared the expression of selected cytokines and KP enzymes, and the levels of selected KP metabolites, in the brain of MIA offspring following a second, acute immune challenge with lipopolysaccharides (LPS) on postnatal day (PND) 35 (adolescence) or PND 60 (early adulthood). Assessed in adolescence, MIA did not alter the expression of pro-inflammatory cytokines (except TNF-α) or KP metabolite levels compared to controls, but substantially reduced the expression of the anti-inflammatory cytokines IL-4 and IL-10 and influenced the expression of two of the four KP enzymes examined (IDO1 and TDO2). LPS treatment caused distinct changes in the expression of pro- and anti-inflammatory cytokines, as well as KP enzymes in MIA offspring, but had no effect on KP metabolites compared to control rats. Several of these effects were blunted in MIA offspring receiving LPS on PND 60. Notably, LPS caused a significant reduction in brain kynurenine levels in these animals. Of relevance for SZ-related hypotheses, these results indicate that MIA leads to an increasingly defective, rather than an overactive, immune regulation of cerebral KP metabolism during the postnatal period.

Indexed as

AnimalsBrainCytokinesDisease Models, AnimalFemaleGene ExpressionInflammationKynurenineLipopolysaccharidesNeurodevelopmental DisordersPoly I-CPregnancyPrenatal Exposure Delayed EffectsRats, WistarCytokinesKynurenineLipopolysaccharidesPoly I-CCytokinesKynurenic acidLipopolysaccharidesPoly I:CTwo hit models

Identifiers

PMID30267854
PMCPMC6249106
OpenAlexW2893120722

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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.