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Peer-reviewedCC BY 4.0Frontiers in Immunology

Neonatal outcomes and immune reprogramming induced by prenatal opioid and hepatitis C exposure

  • Brianna M. Doratt1
  • Heather E. True1
  • Sheridan B. Wagner1
  • Delphine C. Malherbe1
  • Cynthia Cockerham2
  • John O’Brien2
  • Ilhem Messaoudi1
  1. 1Department of Microbiology, Immunology, and Molecular Genetics, College of Medicine, University of Kentucky
  2. 2Department of Obstetrics & Gynecology, College of Medicine, University of Kentucky
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Abstract

Introduction: Prenatal opioid exposure (POE) is an escalating public health concern. However, its impact on neonatal immune development remains poorly defined. This study examined how POE, with or without maternal hepatitis C (hepatitis C virus, HCV) infection, shapes neonatal immunity.

Methods: Umbilical cord blood was collected from pregnancies included uncomplicated term controls (n=38) and deliveries in patients with severe opioid use disorder on medication-assisted treatment, with (n=41) or without HCV (n=34) infection. Flow cytometry was used to characterize cell phenotype and functional response to stimulation. Single-cell RNA sequencing was used to investigate transcriptomics changes.

Results: POE was associated with smaller birth size, higher rates of congenital anomalies, and longer intensive care admissions. Immune profiling showed a proinflammatory milieu, reduced circulating levels of neuroprotective factors, expanded memory/effector T and B cells, blunted T-cell responses, and markedly reduced natural killer (NK) cell frequency and cytotoxicity, especially in POE HCV+ newborns. Monocytes exhibited inflammatory reprogramming with impaired antiviral and tissue repair pathways and disrupted lymphoid–innate immune cell communication.

Discussion: These findings suggest that POE-driven immune disequilibrium may underlie adverse early-life outcomes and highlight monitoring and intervention targets.

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Cite

BibTeXRIS
BibTeX
@article{doratt2026neonatal,
  title = {{Neonatal outcomes and immune reprogramming induced by prenatal opioid and hepatitis C exposure}},
  author = {Brianna M. Doratt and Heather E. True and Sheridan B. Wagner and Delphine C. Malherbe and Cynthia Cockerham and John O’Brien and Ilhem Messaoudi},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1794914},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1794914/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Neonatal outcomes and immune reprogramming induced by prenatal opioid and hepatitis C exposure
AU  - Brianna M. Doratt
AU  - Heather E. True
AU  - Sheridan B. Wagner
AU  - Delphine C. Malherbe
AU  - Cynthia Cockerham
AU  - John O’Brien
AU  - Ilhem Messaoudi
PY  - 2026
DA  - 2026/10/13
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1794914
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1794914/full
AB  - Introduction: Prenatal opioid exposure (POE) is an escalating public health concern. However, its impact on neonatal immune development remains poorly defined. This study examined how POE, with or without maternal hepatitis C (hepatitis C virus, HCV) infection, shapes neonatal immunity.  Methods: Umbilical cord blood was collected from pregnancies included uncomplicated term controls (n=38) and deliveries in patients with severe opioid use disorder on medication-assisted treatment, with (n=41) or without HCV (n=34) infection. Flow cytometry was used to characterize cell phenotype and functional response to stimulation. Single-cell RNA sequencing was used to investigate transcriptomics changes.  Results: POE was associated with smaller birth size, higher rates of congenital anomalies, and longer intensive care admissions. Immune profiling showed a proinflammatory milieu, reduced circulating levels of neuroprotective factors, expanded memory/effector T and B cells, blunted T-cell responses, and markedly reduced natural killer (NK) cell frequency and cytotoxicity, especially in POE HCV+ newborns. Monocytes exhibited inflammatory reprogramming with impaired antiviral and tissue repair pathways and disrupted lymphoid–innate immune cell communication.  Discussion: These findings suggest that POE-driven immune disequilibrium may underlie adverse early-life outcomes and highlight monitoring and intervention targets.
SN  - 1664-3224
ER  -