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Functional analysis of the mannose-binding lectin complement pathway in normal pregnancy and preeclampsia
Dorottya Csuka1, Attila Molvarec, Zoltán Derzsy
1Third Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
Journal of Reproductive Immunology
|October 19, 2010
Summary
The mannose-binding lectin pathway (MBL-MASP2) shows increased activity in normal pregnancy and preeclampsia. However, this study found no direct link between MBL-MASP2 activity and the severity of complement activation in preeclampsia.
Area of Science:
- Immunology
- Obstetrics
- Complement System
Background:
- Preeclampsia is a pregnancy complication marked by hypertension and proteinuria.
- Complement activation is observed in both normal and preeclamptic pregnancies.
- The role of the mannose-binding lectin pathway in preeclampsia requires further investigation.
Purpose of the Study:
- To investigate the involvement of the mannose-binding lectin pathway in initiating complement activation in preeclampsia.
- To compare MBL-MASP2 activity in preeclamptic patients, healthy pregnant women, and non-pregnant women.
Main Methods:
- Functional activity of the mannose-binding lectin-associated serine protease 2 (MBL-MASP2) complex was measured using ELISA.
- Circulating levels of complement components and C-reactive protein (CRP) were quantified.
- Study included 60 preeclamptic patients, 60 healthy pregnant women, and 56 healthy non-pregnant women.
Main Results:
- MBL-MASP2 activity was higher in healthy pregnant women compared to non-pregnant women.
- No significant increase in MBL-MASP2 activity was found in preeclamptic patients versus healthy pregnant women.
- MBL-MASP2 activity did not correlate with complement parameters, clinical data, or CRP levels in preeclampsia.
Conclusions:
- The complement system is activated in normal pregnancy and further in preeclampsia.
- MBL-MASP2 activity increases during normal pregnancy and remains elevated in preeclampsia.
- The mannose-binding lectin pathway appears to play a minor role in the pathological complement activation observed in preeclampsia.
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