A Role for Mannose-binding Lectin, a Component of the Innate Immune System in Pre-eclampsia

Overview

Journal Am J Reprod Immunol

Specialties Allergy & Immunology
Reproductive Medicine

Date 2008 Aug 30

PMID 18727690

Citations 27

Authors

Nandor Gabor Than

Roberto Romero

Offer Erez

Juan Pedro Kusanovic

Adi L Tarca

Samuel S Edwin

Jung-Sun Kim

Sonia S Hassan

Jimmy Espinoza

Pooja Mittal

Shali Mazaki-Tovi

Lara Friel

Francesca Gotsch

Edi Vaisbuch

Natalia Camacho

Zoltan Papp

Affiliations

Soon will be listed here.

Abstract

Problem: Mannose-binding lectin (MBL) is a pattern-recognition receptor that activates complement and modulates inflammation. Homozygosity for the most common allele of the MBL2 gene that is associated with high MBL serum concentrations is more prevalent among patients with pre-eclampsia. The objective of this study was to determine maternal plasma MBL concentrations in normal pregnant women and patients with pre-eclampsia.

Method Of Study: This cross-sectional study included normal pregnant women (n = 187) and patients with pre-eclampsia (n = 99). Maternal plasma MBL concentrations were determined by ELISA.

Results: Women with pre-eclampsia had a higher median maternal plasma MBL concentration than normal pregnant women. MBL concentration distribution curves were three-modal, the subintervals in normal pregnancy were low (< 143.7), intermediate (143.7-1898.9) and high (> 1898.9 ng/mL). The proportion of normal pregnant women was larger in the low subinterval, while the proportion of patients with preeclampsia was larger in the high subinterval (P = 0.02). Normal pregnant women in the high subinterval had a larger rate of placental underperfusion than those in the low and intermediate subintervals (P = 0.02).

Conclusions: The median maternal plasma MBL concentration is elevated in patients with pre-eclampsia and a larger proportion of these patients are in the high subinterval than normal pregnant women, suggesting that this component of the innate immune system is involved in the mechanisms of disease in pre-eclampsia.

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