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Immune Synaptopathy and Sex Differences in Recognition Memory from Neonatal Staphylococcus epidermidis Infection
Wing Ki Chan1, Seyedeh Marziyeh Jabbari Shiadeh2, Janne Lenzig2
1Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden, wing.ki.chan@gu.se.
Developmental Neuroscience
|September 10, 2025
Summary
Neonatal Staphylococcus epidermidis (SE) infection causes long-term, sex-specific changes in recognition memory and brain plasticity. Male mice showed greater vulnerability to these effects, highlighting distinct neurodevelopmental impacts in preterm infants.
Area of Science:
- Neuroscience
- Immunology
- Developmental Biology
Background:
- Staphylococcus epidermidis (SE) is a common cause of hospital-acquired infections in preterm infants, potentially leading to sepsis.
- While short-term neurodevelopmental effects of SE infection are known, long-term impacts on cognitive function and neuronal plasticity remain unclear.
- Early life brain insults can significantly affect sensitive developmental processes, necessitating investigation into SE's lasting consequences.
Purpose of the Study:
- To investigate the long-term effects of postnatal SE infection on recognition memory.
- To analyze the impact of SE infection on hippocampal neuroplasticity and related molecular markers.
- To determine if these effects are sex-specific in a neonatal mouse model.
Main Methods:
- Neonatal C57Bl/6 mice (postnatal day 4) were intraperitoneally injected with SE or saline.
- Recognition memory was assessed using the novel object recognition test (NORT) on postnatal day 45.
- Brain tissue was analyzed for neuronal maturation, synaptic plasticity (spine density), and nerve growth factor (NGF) expression.
Main Results:
- Postnatal SE infection led to sex-specific, long-term alterations in recognition memory and hippocampal neuroplasticity.
- Female mice exhibited enhanced recognition memory, while males showed no significant change; however, both sexes had reduced doublecortin-positive neurons.
- Males displayed increased spine density and disrupted spine organization, along with elevated hippocampal NGF, indicating greater neuroplasticity impairment.
Conclusions:
- Neonatal SE infection induces persistent, sex-specific changes in recognition memory and hippocampal neuroplasticity.
- Male mice demonstrated increased vulnerability to SE-induced neurodevelopmental disruptions.
- Findings suggest distinct neurodevelopmental trajectories following early-life immune challenges, impacting sex-specific cognitive outcomes in preterm infants.
