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Complement activation: a critical mediator of adverse fetal outcomes in placental malaria?

Andrea L Conroy1, Chloe R McDonald, Karlee L Silver

  • 1Sandra A. Rotman Laboratories, McLaughlin-Rotman Centre for Global Health, University Health Network-Toronto General Hospital, University of Toronto, Toronto, M5G 1L7, Canada.

Trends in Parasitology
|April 16, 2011
PubMed

Malaria infection is a significant risk factor for low birth weight outcomes in pregnancy. Despite efforts to define the molecular mechanisms that cause low birth weight as a result of intrauterine growth restriction, the roles of inflammation and mononuclear cells in the process are incompletely understood. Data from adverse pregnancy outcomes in humans and from murine models of pathological pregnancies suggest that C5a could be an important upstream regulator of placental angiogenesis, and excessive C5a could lead to functional placental insufficiency by impairing adequate vascularization of the placenta. Based on recent evidence, we hypothesize that complement factor C5a is a central initiator of poor birth outcomes associated with placental malaria by promoting mononuclear cell migration, activation and dysregulated angiogenesis.

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