Maternal listeria monocytogenes infection induces placental stress and histological alterations in rat embryos
1 Department of Biology, College of Education for Pure Science, University of Kirkuk, Kirkuk, Iraq.
2 Department of Biology, College of Education for Pure Sciences, University of Samarra, Salah al-Din, Iraq.
Research Article
Open Access Research Journal of Life Sciences, 2026, 11(02), 086–095.
Article DOI: 10.53022/oarjls.2026.11.2.0010
Publication history:
Received on 06 March 2026; revised on 07 April 2026; accepted on 13 April 2026
Abstract:
Background: Listeria monocytogenes is a gram-positive intracellular pathogen that causes serious pregnancy complications, such as fetal loss, preterm birth, and listeriosis in the neonatal stage. The pathogen has an outstanding placental tropism and exploits the pathways of trophoblast invasion to interfere with the fetal growth.
Hypothesis: The hypothesis was to examine the impact of maternal infection with L. monocytogenes on the placental and liver expression of inflammatory cytokines, the oxidative stress parameters, the fetal morphometric outcomes in Wistar rat model.
Methods: Thirty pregnant Wistar rats (n = 10 each) were put into three groups (Group A: control, Group B: low-dose infection: 1 × 10 3 CFU/mL, and Group C: high-dose infection: 1 × 10 5 CFU/mL) and inoculated on gestational day 7 intraperitoneally. liver and placental tissues were harvested on day 20. Cytokines (TNF-α, IL-6), oxidative stress (MDA, SOD, CAT, GSH), fetal morphometry, and histological examinations were performed.
Findings: The fetal viability reduced in the high-dose group compared to controls, with increased resorptions. There was a significant decrease in fetal body weight and crown-rump length in the infected groups. Placental and fetal hepatic tissues exhibited a dose-dependent increase in inflammatory cytokines (TNF-α and IL-6) and oxidative stress markers, alongside a significant depletion of antioxidant enzymes (SOD, CAT, and GSH) in both tissues. Furthermore, histological examination of fetal liver confirmed severe structural alterations, including hepatocyte necrosis, vacuolization, and inflammatory cell infiltration
Conclusion: Maternal infection with L. monocytogenes triggers dose dependent inflammatory and oxidative cascade in the placenta and liver, resulting in poor fetal development and high embryonic loss. These results bring to the fore the importance of microbiological screening and specific anti-inflammatory interventions in pregnancy.
Keywords:
Listeria monocytogenes; Placental Inflammation; Oxidative Stress; Fetal Morphometry; TNF-Α; IL-6; Rat Model; Reproductive Toxicology
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