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Sequential Exposure to Histological Chorioamnionitis and Postnatal Hyperoxia Alters Gene Expression in Cord Blood Monocytes

ABSTRACT: Sequential exposure to histological chorioamnionitis and postnatal hyperoxia induces alterations in gene expression and molecular pathways in neonatal cord blood monocytes, affecting immune regulation, which could potentially contribute to the pathogenesis of short- and long-term diseases in neonates. We have used microarray to find the global gene expression in neonatal cord blood monocytes exposed to either histological chorioamnionitis (HCA) or hyperoxia or both compared to control samples (no-HCA)

ORGANISM(S): Homo sapiens

PROVIDER: GSE346094 | GEO | 2026/09/03

REPOSITORIES: GEO

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Project description:Bronchopulmonary dysplasia (BPD) arises from a combination of prenatal and postnatal environmental factors, but the impact of prenatal inflammation on subsequent postnatal lung injury remains unclear. We aimed to investigate how prenatal lipopolysaccharide (LPS)-induced chorioamnionitis alters the composition of resident pulmonary immune cells and modifies the response to hyperoxia-induced lung injury in neonatal rats. Pregnant Sprague-Dawley rats received intra-amniotic injections of LPS or normal saline (NS) at embryonic day 20. Pups were euthanized on postnatal day 1 (P1) or exposed to 85% oxygen (O₂) or room air (RA) for 14 days and euthanized on postnatal day 14 (P14) for analysis. Resident pulmonary immune cells were quantified by flow cytometry. Mann–Whitney and ANOVA tests were used for group comparisons (p<0.05). mRNA from pulmonary immune cells collected on P1 was subjected to RNA sequencing and differential gene expression analysis. On P1, prenatal LPS exposure did not change the overall percentage of CD45⁺ pulmonary immune cells but decreased the percentages of CD3⁺CD4⁺ T cells, CD3⁺CD8⁺ T cells, and CD45R⁺ B cells compared with the NS+RA group. In contrast, CD161⁺ NK cells and CD43⁺ monocytes were significantly increased. Upregulated genes were enriched in inflammatory biological processes. By P14, cell composition in the LPS+RA group normalized. However, a second insult with postnatal hyperoxia resulted in an increased proportion of CD161⁺ NK cells in the LPS+O₂ group only and an increased proportion of CD43⁺ monocytes in the NS+O₂ group only, with a relative reduction in monocytes in the LPS+O₂ group at P14. In this rat model of BPD, LPS-mediated in-utero inflammation primes neonatal lung immune cells for a dysregulated response to postnatal hyperoxia. Dual prenatal and postnatal injuries result in persistent elevation of NK cells and reduction of monocytes, while other immune subsets respond differentially, suggesting that prenatal events condition the neonatal lung immune system in ways that may influence BPD pathogenesis.

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Sequential Exposure to Histological Chorioamnionitis and Postnatal Hyperoxia Alters Gene Expression in Cord Blood Monocytes

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