Abstract

Share on facebook
Share on twitter
Share on linkedin

The effect of inflammation and variable hyperoxia on developing white matter

Presented at the Neonatal Society 2010 Autumn Meeting.

Pilley E, Wade J, Gillespie T, Laing IA, Becher JC

Jennifer Brown Research Laboratory, Centre for Reproductive Biology, QMRI, University of Edinburgh

Background: Epidemiological and experimental studies show that hyperoxia and infection are independently associated with injury to the developing brain (1-3). Moreover inflammation may precondition the fetal brain resulting in increased or decreased injury when exposed to subsequent hypoxia-ischaemia (4). We examined the combined effects of antenatal bacterial endotoxin and postnatal variable hyperoxia on the developing rodent white matter.

Methods: Pregnant rats received intraperitoneal lipopolysaccharide (225mcg/kg) or saline on E18 and E19. Dams and their pups were then reared in room air or fluctuating hyperoxia (circa 10kPa) for seven days. Pup brains were examined at P7 for myelin basic protein (MBP) and glial fibrillary acidic protein (GFAP), a marker of astrogliosis, in the internal and external capsules using immunohistochemistry. Quantification of both MBP and GFAP mRNA was also undertaken.

Results: Pups exposed to antenatal LPS alone showed a significant decrease in MBP at P7 (p<0.001) but there was an increase in MBP mRNA expression. This increase in MBP mRNA was suppressed where pups who had been exposed to antenatal LPS were then reared in variable hyperoxia. LPS caused a significant increase in GFAP mRNA expression (p<0.001), which was further increased where pups were reared in variable hyperoxia (p<0.05). Postnatal variable hyperoxia had little effect on myelination at P7 (immunohistochemistry) but MBP mRNA was decreased (P<0.05).

Conclusion: These results show that antenatal inflammation reduces myelination in the motor tracts of the developing brain. The increase in MBP mRNA production suggests that hypomyelination induced by endotoxin may be transient and potentially reversible. Subsequent postnatal variable hyperoxia results in suppression of MBP mRNA expression and increases GFAP mRNA production. Where preterm infants are exposed to antenatal inflammation, hyperoxia may continue to disrupt myelination postnatally.

Corresponding author: elizabeth.pilley@ed.ac.uk

References
1. Wu Ment Retard Dev Disabil Res Rev 2002
2. Cai et al Pediatr Res 2000
3. Felderhoff-Mueser et al Neurobiol Dis 2004
4. Eklind et al Eur J Neurosci 2001

More to explorer

2020 Spring Meeting

The Spring Meeting of the Neonatal Society has been cancelled due to COVID-19 Dear member, After careful consideration we have decided to

2019 Autumn Meeting

7th November 2019 The Royal Society of Medicine, London 9:30 – 17:30 with a drinks Reception at 18:00 Open to all professionals

2019 Summer Meeting

60th anniversary celebration This special meeting marked the 60th anniversary of the founding of the Neonatal Society. A series of keynote lectures

Search by category
Scroll to Top

We use cookies to ensure that we give you the best possible experience on our website. By continuing to browse the site you are agreeing to the use of cookies from The Neonatal Society.