Evidence map›Paper›PMID 42755417›Full record

ArticleDevelopmental neurobiology2026

Maternal and Postnatal Effects of Poly I:C-Induced Intrauterine Inflammation and Rytvela, a Non-Competitive IL-1R Antagonist, in the Pregnant Spiny Mouse.

Nhi T Tran, Rachid Kamareddine, Nadia Bellofiore, David M Olson, Sylvain Chemtob, Sarah A Robertson, Jeffrey A Keelan, Stacey J Ellery

Abstract read
In one paragraph

Article in Developmental neurobiology, 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. Article
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

8 authors.

Nhi T TranThe Ritchie Centre, Department of Obstetrics and Gynaecology, Monash University, Clayton, Victoria, Australia.
Rachid KamareddineThe Ritchie Centre, Department of Obstetrics and Gynaecology, Monash University, Clayton, Victoria, Australia.
Nadia BellofioreThe Ritchie Centre, Department of Obstetrics and Gynaecology, Monash University, Clayton, Victoria, Australia.
David M OlsonDepartments of Obstetrics and Gynecology, Pediatrics, and Physiology, University of Alberta, Edmonton, Alberta, Canada.
Sylvain ChemtobDepartment of Pharmacology and Physiology, Université de Montréal, Research Center, CHU Sainte-Justine, Montreal, Quebec, Canada.
Sarah A RobertsonSchool of Pharmacy and Biomedical Science, Adelaide University, Adelaide, South Australia, Australia.
Jeffrey A KeelanSchool of Biomedical Sciences, University of Western Australia, Perth, Australia.
Stacey J ElleryThe Ritchie Centre, Department of Obstetrics and Gynaecology, Monash University, Clayton, Victoria, Australia.

Funding

Australian NHMRC Project Grant 1145295National Health and Medical Research Council 1145295
6 · The paper itself

Abstract

Maternal infection-induced inflammation during pregnancy is associated with adverse neurodevelopment. Rytvela, an allosteric IL-1 receptor antagonist, reduces IL-1β-mediated pathology in fetal rodents and sheep. However, its effects on TLR3-mediated inflammation and subsequent offspring growth and behavior remain unclear. Using precocial spiny mice, the primary outcome of this study was to examine whether rytvela could attenuate the acute maternal inflammatory response to mid-gestation exposure to polyinosinic:polycytidylic acid (Poly(I:C)). Secondary offspring outcomes included postnatal growth and behavior. At gestational day 20 (term = 39 days), pregnant mice received two intraperitoneal injections, 4 h apart, of saline (0.9% w/v, n = 14), Poly(I:C) (12 mg/kg, n = 14), or Poly(I:C) + rytvela (12 mg/kg + 3 mg/kg, respectively, n = 14). Ten dams/group were culled 8 h after dose 1 to assess inflammatory responses. The remainder (n = 4 dams/group) were delivered at term. Offspring (control n = 7, Poly(I:C) n = 8, Poly(I:C) + rytvela n = 11) growth was monitored and behavioral testing undertaken from postnatal day (PND) 3-45. Poly(I:C) increased maternal serum (p = 0.01) and amniotic fluid (p = 0.003) IL-1β, and upregulated Il1b, Il6 and Tnf expression in the spleen and thymus. Rytvela reduced IL-1β levels but did not attenuate elevated cytokine gene expression. Poly(I:C) slowed postnatal growth (PND 18-27, p < 0.05), which recovered earlier with rytvela. Poly(I:C) exposure did not alter offspring behavior in tests completed to PND 45. However, Poly(I:C) + rytvela offspring showed reduced locomotor activity (distance: p < 0.001; velocity: p = 0.021). In conclusion, rytvela attenuated the primary inflammatory response to Poly(I:C), promoting earlier postnatal growth recovery despite persistent cytokine gene expression. Reduced locomotor activity after prenatal rytvela exposure warrants further investigation.

Indexed as

InflammationInterleukin 1 Receptor Antagonist ProteinPoly I-CPrenatal Exposure Delayed EffectsReceptors, Interleukin-1AnimalsAnimals, NewbornFemaleMicePregnancyInterleukin 1 Receptor Antagonist ProteinPoly I-CReceptors, Interleukin-1behaviorcognitive functioncytokinesmaternal immune challengeoffspring growthpregnancy

Identifiers

PMID42755417
PMCPMC13586770

What OpenQuestion holds

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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.