Effects of maternal smoking in mice on markers of brain inflammation and hypoxia in male offspring  — The Association Specialists
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Effects of maternal smoking in mice on markers of brain inflammation and hypoxia in male offspring  (376)

Yik Lung YLC Chan 1 , Ibrahim Al-Odat 1 , Nicole Jones 2 , Hui Chen 1
  1. School of Medical and Molecular Biosciences, Faculty of Science, University of Technology, Sydney, Ultimo, NSW, Australia
  2. School of Medical Sciences, Faculty of Medicine, University of New South Wales, Sydney, New South Wales, Australia

Objective: Maternal smoking can cause long lasting adverse effects on the structural and functional development of fetal brain. However, the impact of maternal smoke exposure (SE) on markers of inflammation and hypoxia in offspring brain is unknown.

Methods: Female Balb/c mice were exposed to cigarette smoke (2 cigarettes twice/day) for 6 weeks prior to mating, during pregnancy and lactation; the control mice were exposed to normal room air. Male pups were sacrificed at postnatal day (P) 1, P20 and 13 weeks. The brain markers of inflammation and hypoxia were measured using rt-PCR and Western blotting.

Results: mRNA expression of the inflammatory marker interleukin (IL)-1 receptor was increased at P1, P20 and 13 weeks in the SE offspring compared with age matched controls. IL-6 mRNA was only increased at 13 weeks in the SE offspring. Expression of tumor necrosis factor (TNF) α and toll like receptor (TLR) 4 mRNA were reduced in the SE offspring at P1, but not at P20. At 13 weeks, TLR4 mRNA was upregulated in the SE offspring; however, there was no change in TNFα. Hypoxia-inducible factor-1 (HIF-1) α mRNA levels were not changed at P1, but increased in the SE offspring at P20 and 13 weeks. Similar changes in HIFα protein levels over the time course were observed. Early growth response protein 1 can regulate inflammation in response to ischemia, which also works together with HIFα to reduce ischemic injury. Its expression was only increased at P20 in the SE offspring.

Conclusion: Maternal SE reduced the expression of inflammatory markers at P1, however leads to increased inflammatory response in offspring in adulthood. Markers of hypoxia were also high in mature offspring.  Further study is needed to determine whether these changes in the brain will render the offspring to more vulnerable to brain damage.