Publications & Reports

Placental hypoxia during placental malaria.

Philippe Boeuf, Aimee Tan, Cleofe Romagosa, Jane Radford, Victor Mwapasa, Malcolm E Molyneux, Steven R Meshnick, Nicholas H Hunt, Stephen J Rogerson
Department of Medicine, University of Melbourne, Parkville, Victoria, Australia.


BACKGROUND: Placental malaria causes fetal growth retardation (FGR), which has been linked epidemiologically to placental monocyte infiltrates. We investigated whether parasite or monocyte infiltrates were associated with placental hypoxia, as a potential mechanism underlying malarial FGR. METHODS: We studied the hypoxia markers hypoxia inducible factor (HIF)-1alpha, vascular endothelial growth factor (VEGF), placental growth factor, VEGF receptor 1 and its soluble form, and VEGF receptor 2. We used real-time polymerase chain reaction (in 59 women) to examine gene transcription, immunohistochemistry (in 30 women) to describe protein expression, and laser-capture microdissection (in 23 women) to examine syncytiotrophoblast-specific changes in gene expression. We compared gene and protein expression in relation to malaria infection, monocyte infiltrates, and birth weight. RESULTS: We could not associate any hallmark of placental malaria with a transcription, expression, or tissue-distribution profile characteristic of a response to hypoxia, but we found higher HIF-1alpha levels (P= .0005) and lower VEGF levels (P= .0026) in the syncytiotrophoblasts of cases of malaria than in those of asymptomatic control placentas. CONCLUSIONS: Our data are inconsistent with a role for placental hypoxia in the pathogenesis of malaria-associated FGR. The laser-capture microdissection study was small, but its results suggest (1) that malaria affects syncytiotrophoblast-gene transcription and (2) novel potential mechanisms for placental malaria-associated FGR.


  • Journal: The Journal of Infectious Diseases
  • Published: 01/03/2008
  • Volume: 197
  • Issue: 5
  • Pagination: 757-765


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