Mannose-binding lectin genotypes are associated with shorter gestational age. An evolutionary advantage of low MBL production genotypes?
Molecular Immunology , Volume 45 - Issue 5 p. 1514- 1518
Background: The complement factor mannose-binding lectin (MBL) is associated with adverse pregnancy outcome. MBL serum concentrations are increased from early pregnancy onwards and depend upon several gene polymorphisms. We investigated whether MBL polymorphisms are associated with term and preterm birth, since preterm birth is the leading cause of neonatal morbidity and mortality. Methods: MBL2 gene polymorphisms were determined in 157 nulliparous women. Considering MBL polymorphisms cases were categorized in groups of high (A), intermediate (B) and low (C) MBL production. Kaplan-Meier survival and multiple linear regression analysis were performed. Results: Women with high MBL genotype group A had a shorter gestational age (274 days ± S.D. 21) than the women with the intermediate MBL genotype group B (283 days ± S.D. 12) and the low MBL genotype group C (284 days ± S.D. 9). This difference in mean gestational age is almost totally attributable to premature births in group A, since 12 of the 14 preterm births were from women with the high MBL genotype group A and only two from the intermediate MBL genotype group B. Conclusions: We found an association between the maternal high MBL genotype group A and premature birth, suggesting that during pregnancy MBL-associated inflammation caused by higher MBL activity may contribute to earlier delivery. Furthermore, this finding might explain why so many individuals are MBL deficient in the general population.
|Gestational age, Mannose-binding lectin, Polymorphisms, Preterm birth|
|Organisation||Erasmus MC: University Medical Center Rotterdam|
Geijn, F.E, Dolhain, R.J.E.M, van Rijs, W, Willemsen, S.P, Hazes, J.M.W, & de Groot, C.J.M. (2008). Mannose-binding lectin genotypes are associated with shorter gestational age. An evolutionary advantage of low MBL production genotypes?. Molecular Immunology, 45(5), 1514–1518. doi:10.1016/j.molimm.2007.08.021