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Related Concept Videos

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Related Experiment Video

Updated: Apr 27, 2026

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Prenatal dexamethasone exposure in rats results in long-term epigenetic histone modifications and tumour necrosis

Hong-Ren Yu1, Ho-Chang Kuo, Chih-Cheng Chen

  • 1Department of Paediatrics, Chang Gung Memorial Hospital-Kaohsiung Medical Centre, Graduate Insititute of Clinical Medical Science, Chang Gung University College of Medicine, Kaohsiung, Taiwan.

Immunology
|June 26, 2014
PubMed
Summary

Prenatal glucocorticoid (GC) exposure, like dexamethasone (DEX), can alter fetal immune development. This study shows lasting immune system changes in adult rats, impacting inflammation and epigenetic modifications.

Keywords:
epigeneticprenatal glucocorticoidtumour necrosis factor-α

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Area of Science:

  • Immunology
  • Developmental Biology
  • Pharmacology

Background:

  • Glucocorticoids (GCs) are used to accelerate fetal lung maturation before preterm birth.
  • Limited data exists on the long-term effects of prenatal GC exposure on immune system development.
  • Previous studies suggest minimal impact, but effects in later childhood remain unclear.

Purpose of the Study:

  • To investigate the long-term impact of prenatal dexamethasone (DEX) exposure on immune programming in offspring.
  • To determine if prenatal GC exposure affects immune responses and epigenetic modifications in adult rats.

Main Methods:

  • Pregnant Sprague-Dawley rats received DEX or saline during late gestation.
  • Offspring spleens were analyzed at early postnatal (day 7) and adult (day 120) stages.
  • Gene expression of inflammation mediators and splenocyte cytokine production post-stimulation were assessed.

Main Results:

  • Prenatal DEX reduced mRNA levels of MMP-9, TNF-α, and GM-CSF early post-birth.
  • Adult rats exposed to prenatal DEX showed reduced TNF-α production upon stimulation.
  • Decreased histone acetylation in the TNF-α promoter correlated with reduced TNF-α expression.

Conclusions:

  • Prenatal DEX exposure exerts a profound and lasting influence on the developing immune system, extending into adulthood.
  • Epigenetic modifications, specifically histone modifications in the TNF-α promoter, play a role in regulating immune responses following prenatal DEX exposure.