Article

Dysregulated Complement Activation as a Common Pathway of Injury in Preeclampsia and Other Pregnancy Complications

Department of Obstetrics and Gynecology, University of Colorado Denver School of Medicine, Aurora, CO 80045, USA.
Placenta (Impact Factor: 2.71). 07/2010; 31(7):561-7. DOI: 10.1016/j.placenta.2010.03.010
Source: PubMed

ABSTRACT

The complement system protects the host against invading organisms, initiates inflammation and dispose of immune complexes and the products of inflammatory injury. The complement system provides an important link between the innate and adaptive immune systems. Experimental observations suggest that increased complement activation causes and/or perpetuates inflammation during pregnancy. Recent studies suggest a link between complement activation and preeclampsia. Excessive activation or insufficient regulation of complement recruits leukocytes and unleashes potent inflammatory and anti-angiogenic mediators associated with placental insufficiency and maternal endothelial dysfunction characteristic of preeclampsia. We review the animal and human studies that link complement activation and pathogenic events in preeclampsia, present evidence that activation of the complement system is associated with the development of preeclampsia and provides new targets to prevent its complications.

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    • "Like CD46 and CD55, complement Factor H (CFH) is a soluble plasma regulator of the activation of the complement cascade that limit activation of the alternative pathway, more specifically by targeting C3 convertase (Kolev et al., 2014 ). Data on CFH levels during pregnancy is scant and the role of CFH in pregnancy is uncertain (Lynch and Salmon, 2010). Johnson and Gustavii (1987) measuring plasma CFH with electroimmuno assay in 72 healthy pregnant women at 8–14, 24–26, 35–38 weeks of pregnancy and at delivery, reported that mean levels of CFH increase as the pregnancy progress. "

    Full-text · Dataset · Feb 2016
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    • "Like CD46 and CD55, complement Factor H (CFH) is a soluble plasma regulator of the activation of the complement cascade that limit activation of the alternative pathway, more specifically by targeting C3 convertase (Kolev et al., 2014). Data on CFH levels during pregnancy is scant and the role of CFH in pregnancy is uncertain (Lynch and Salmon, 2010). Johnson and Gustavii (1987) measuring plasma CFH with electroimmuno assay in 72 healthy pregnant women at 8–14, 24–26, 35–38 weeks of pregnancy and at delivery, reported that mean levels of CFH increase as the pregnancy progress. "
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    • "That a single signaling pathway could account for this vascular phenotype induced by malaria is attractive for the development of therapeutic interventions. These findings may also have broad implications for other pregnancy complications associated with immune activation and placental insufficiency (e.g., preeclampsia), where both C5a and sFlt-1 have been associated with adverse birth outcomes (Lynch and Salmon, 2010). "
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