Evidence map›Paper›PMID 40451148›Full record

ArticleDevelopmental neuroscience2026

Chorioamnionitis Induces a Unique Time Course of Inflammatory Changes and Immune Reponses in the Brain and Spleen.

Maide Ozen, Alexandria Vergara, Yuma Kitase, Balaji Vijayakumar, Aidan Perales, Shenandoah Robinson, Lauren L Jantzie

Abstract read
In one paragraph

Article in Developmental neuroscience, 2026. 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

7 authors.

Maide OzenNeonatal-Perinatal Medicine, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA, mozen1@jhmi.edu.
Alexandria VergaraNeonatal-Perinatal Medicine, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Yuma KitaseNeonatal-Perinatal Medicine, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Balaji VijayakumarNeonatal-Perinatal Medicine, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Aidan PeralesNeonatal-Perinatal Medicine, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Shenandoah RobinsonDepartment of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Lauren L JantzieNeonatal-Perinatal Medicine, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

Funding

Sleep and Circadian Dysfunction, Brain and Neurobehavioral Development in AutismP50HD103538 · NICHD · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI S. Ali Fatemi, Bradley L Schlaggar · 2020 to 2026
$9.9M
Placental Mediated Mechanisms of Perinatal Brain InjuryR01HL139492 · NHLBI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI JANTZIE, LAUREN LEIGH COONEY · 2018 to 2021
$1.6M
The role of chorioamnionitis-induced perinatal alterations of Heme-oxygenase-1 (HO-1) pathway on neuroinflammation and neonatal white matter injuryK08HD107166 · NICHD · JOHNS HOPKINS UNIVERSITY · PI Maide Ozen · 2022 to 2026
$859k
Cytek Aurora full spectrum flow cytometric analyzerS10OD026859 · OD · JOHNS HOPKINS UNIVERSITY · PI WANG, ZACK Z. · 2019 to 2019
$242k
NHLBI NIH HHS R01 HL139492NICHD NIH HHS K08 HD107166NICHD NIH HHS P50 HD103538NIH HHS S10 OD026859
6 · The paper itself

Abstract

introductionInflammatory oxidative microenvironments can alter heme oxygenase-1 (HO-1) homeostasis. Dysregulation of HO-1 favors proinflammatory signals, while transferrin receptor 1 (TfR1) regulates anti-inflammatory signal transduction. Previously, we have shown that chorioamnionitis (CHORIO) induces sustained elevations in HO-1/TfR1 at postnatal day (P)2 and mononuclear cell-driven inflammation at term age equivalent P7. Here, we hypothesized that an altered HO-1/TfR1 developmental time course would coincide with inflammatory/immune signal changes in the brain.

methodsTo induce CHORIO in rats, we performed a laparotomy followed by bilateral transient uterine artery occlusion and intra-amniotic injection of lipopolysaccharide (LPS) at E18. The control group received laparotomy only with equivalent duration of anesthesia. We used real-time polymerase chain reaction (RT-PCR), multiplex electrochemiluminescent immunoassay (MECI), and flow cytometry (FC) to study changes in pro- and anti-inflammatory gene expression, immune cell secretome, and immune cells at critical and clinically relevant timepoints following CHORIO.

resultsWe found an acute reduction in anti-inflammatory signals in the cortex on embryonic day (E)19. This was followed by an increased proinflammatory signature on postnatal day (P)2. There were also significant alterations in the phenotypic distribution of splenic T cells on P7, a key organ in immune function. Furthermore, we showed that the microenvironment of the cortex at P21 was skewed toward a proinflammatory state by significant increases in IL-6. The prominence of T-helper cells (Th) in brain concomitant with a proinflammatory state at P21 suggests emerging inflammation and potential for neural injury.

conclusionsDefining how these and other inflammatory/immune signatures contribute to perinatal brain injury and investigating distinct immune signatures at more developmental time courses will be beneficial for targeting emerging therapies.

Indexed as

BrainChorioamnionitisInflammationSpleenAnimalsFemaleHeme Oxygenase-1PregnancyRatsRats, Sprague-DawleyReceptors, TransferrinHeme Oxygenase-1Receptors, TransferrinHemeImmune cellInflammationNeuroimmune functionPerinatal brain injuryTfR1

Identifiers

PMID40451148
PMCPMC12281413

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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.