Mannose-binding lectin may affect pregnancy outcome (original) (raw)
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Mannose-binding lectin levels during pregnancy: a longitudinal study
Human Reproduction, 2006
BACKGROUND: Pregnancy is associated with changes in the immune system. Although previous studies have focussed mainly on adaptive immunity, there are indications that components of innate immunity, such as mannosebinding lectin (MBL), are associated with pregnancy outcome. Although this would suggest that pregnancy also involves adaptations in innate immunity, there are few studies in this area. Therefore, we aimed to determine whether MBL concentrations and the following steps in complement pathway activation are influenced by pregnancy. METHODS: MBL and Ficolin-2 concentrations, MBL-MBL-associated serine protease (MASP) complex activity, MBL pathway activity and classical complement pathway activity were determined by enzyme-linked immunosorbent assay (ELISA) in sera from pregnant women (n = 32) during each trimester and post-partum. MBL genotyping was performed by PCR. RESULTS: During pregnancy, MBL concentrations increased to 140% [interquartile range (IQR) 116-181%, P < 0.0001]. This increase was already present at 12 weeks of pregnancy and was most pronounced in the high-production AA-genotype. Directly Post-partum MBL concentrations dropped to 57% of baseline (IQR 44-66%, P < 0.0001). Variations in MBL levels were reflected by similar changes in the following steps of complement activation, r > 0.93 (P < 0.01). Ficolin-2 levels and classical complement pathway activity were not similarly influenced by pregnancy. CONCLUSIONS: Pregnancy and the post-partum period profoundly influence MBL serum concentration and MBL complement pathway activity.
Genetics in Medicine, 2006
Human mannose-binding lectin, encoded by the MBL2 gene, is an important component of innate immunity and an important regulator of inflammatory processes. MBL2 gene polymorphisms are associated with an increased risk of neonatal infections and some data suggest a relation between the maternal MBL2 genotype and the risk of premature delivery. In this study, we evaluated whether there is an association between the fetal MBL2 genotype and prematurity. Methods: A microarray-based on-chip PCR method was used to simultaneously detect five common MBL2 polymorphisms (codon 52, 54, 57; promoter-550,-221) in 204 DNA samples isolated from archival blood cards. MBL2 genotypes of infants born before the 36 th week of pregnancy (N ϭ 102) were compared to a control group of infants born at term after the 37 th week (N ϭ 102). Results: The frequency of the codon 52 polymorphism was significantly higher in the pre-term group compared to the term group (10.8% versus 4.9%, P ϭ 0.04), while the frequency of the codon 54 polymorphism was equal in both groups (11.3% versus 11.8%). Interestingly, carriers of genotypes (O/O) likely conferring deficient MBL plasma levels were more common in the group of premature birth (9.8% versus 2.9%, P ϭ 0.05), while the promoter-550 C/C genotype was underrepresented in the pre-term birth group (24.5% versus 39.2%, P ϭ 0.03). Conclusion: Our data add to the knowledge about genetic predisposition to prematurity and suggest that the fetal MBL2 genotype might be an additional genetic factor contributing to the risk of premature delivery.
Journal of Pure and Applied Microbiology
To analyzes the association between Mannose binding lectin MBL gene and preterm labor, DNA was obtained from peripheral blood of 150 aborted women patients diagnosed as preterm labor and 150 healthy individual have no previous preterm history was extracted. Mannose binding lectin gene was genotyped by PCR-RFLP (Polymerase Chain Reaction-Restriction Fragment Length Polymorphism) method. The data were analyzed by odd ratio (OR) calculation with confidence intervals (CI 95%) and chi square x 2 results were statically analysis. Statistical significant were sent as p value ≤0.05. The allelic frequency between gene and preterm labor group was (94.5) in control compared with (70.7) in patients with significant differences. The homozygous were found to be more than heterozygous (32.3) whereas homozygous AA (43.4) and GG (33.3) with significant differences this work is considered the first study for understanding the correlation between Preterm birth and mannose protein level in Iraq .
Mannose-binding lectin-2 genotypes and recurrent late pregnancy losses
Human Reproduction, 2009
background: Low levels of mannose-binding lectin (MBL) predispose to various infectious and inflammatory disorders and have been reported to be associated with recurrent early miscarriages. Recurrent late pregnancy losses (RLPL) in the second trimester is a rare but devastating syndrome where maternal rather than fetal causes are likely to play a stronger role than in early recurrent miscarriage. methods: We identified 75 patients with at least two late losses of pregnancies with apparently normal fetuses between gestational week 14 and 30 among patients with recurrent pregnancy losses referred to our clinic. Polymorphisms in the MBL2 gene associated with plasma MBL levels were investigated in all patients and in 104 women with two or more children and no miscarriages. The patients were divided into three groups: one with clinical signs of cervical insufficiency, one positive for the lupus anticoagulant (LAC) and an idiopathic group.
Mannose-binding lectin in term newborns and their mothers: Genotypic and phenotypic relationship
Human Immunology, 2008
Functional mannose-binding lectin (f-MBL) plays an important role in the innate neonatal immune system. We studied the origin of f-MBL in umbilical cord blood (UCB) by measuring maternal MBL (n ϭ 47), collected before elective cesarean section, and neonatal MBL (n ϭ 43) in arterial umbilical cord blood. In a subgroup, arterial and venous UCB MBL levels were measured. In addition, MBL expression was correlated with genetic mutations. The f-MBL levels in term infants were lower than in their mothers (0.70 g/ml vs 1.11 g/ml, p Ͻ 0.01) and maternal and neonatal MBL levels were only weakly correlated (R ϭ 0.32, p Ͻ 0.001), which suggests a fetal origin of f-MBL. Arterial and venous UCB median MBL levels did not differ (0.98 g/ml vs. 1.40 g/ml, p ϭ 0.20). No homozygous mutations were found. MBL was lower in mothers and infants with a (compound) heterozygous mutation than in those with a wild type. One new (HYPB) and two rare haplotypes (HXPA, LYPD) were reported in our population. Levels of MBL differed depending on the genotype of the mother or the infant. Because the role of MBL in host defense is still unclear, both f-MBL and haplotype should be measured to determine the clinical implications of MBL deficiency in infants.
Mannan-Binding Lectin Deficiency is Associated with Unexplained Recurrent Miscarriage
Scandinavian Journal of Immunology, 1999
Christiansen OB, Kilpatrick DC, Souter V, Varming K, Thiel S, Jensenius JC. Mannan-Binding Lectin Deficiency is Associated with Unexplained Recurrent Miscarriage. Scand J Immunol 1999;49:193-196 Mannan-binding lectin (MBL) is a plasma protein which, upon binding to microbial carbohydrate structures, elicits activation of the complement system. The level of MBL is genetically determined. It has been reported that the frequency of low plasma levels of MBL is increased in patients with unexplained recurrent miscarriages (RM). In the present study plasma MBL levels were determined in 146 Danish women with RM and 41 of their husbands together with 49 Scottish RM women and 41 of their husbands. In both countries MBL levels were also investigated in a total of 444 controls. Based on the control data, a cut-off MBL level < 50 ng/ml was selected to define MBL deficiency. The typical odds ratio for MBL deficiency among female patients in the two populations was 1.68 (95% confidence limits 1.01-2.80, P < 0.05) whereas it was 1.57 (95% confidence limits 0.72-3.42, not significant) for the male partners of the patients. There was a significant correlation between the frequency of MBL deficiency in RM women and the number of previous miscarriages (P < 0.01), whereas no such correlation was found in the husbands. The results indicate that maternal MBL deficiency is associated with RM. Maternal MBL deficiency might impair the immune defence against microorganisms at the feto-maternal interface.
Association Between Mannose‐Binding Lectin Gene Polymorphisms and Pre‐eclampsia in Brazilian Women
American Journal of …, 2010
pregnancy has been associated with disorders such as pre-eclampsia (PE), short gestation period, and miscarriages. 5,6 Inflammatory cells and immunological mediators, such as components of the complement system, are present in the uterine environment. The development of PE, a disorder that leads to high maternal and fetal mortality, involves inflammatory events and a spectrum of clinical presentations, including an incorrect placentation. 1,7-10 PE is characterized by abnormal vascular response to placentation, increased systemic vascular resistance,
PloS one, 2017
Studies on the influence of mannose-binding lectin (MBL) deficiency on infection susceptibility in preterm infants have yielded controversial results. We investigated the association of genotype-based MBL levels with outcome in very-low-birth weight infants (VLBWI). We genotyped 3 genetic variants of MBL2 (rs1800450, rs1800451, rs5030737) in 6878 VLBWI. MBL plasma levels were categorized as normal (wild type, A/A), low (heterozygotes, A/O) or undetectable (homozygotes, O/O). Primary outcome was the effect of genotype-based MBL2 levels on blood-culture proven and clinical sepsis during primary stay in hospital. We also evaluated burden of infection within 24 months after discharge. We found no association between MBL levels and sepsis risk in the whole cohort. Infants without measurable MBL levels born between 32 0/7 to 36 6/7 weeks of gestation, however, had a higher rate of Gram-negative sepsis than infants with normal or reduced MBL levels. In a follow-up investigation at 24 month...
Human Immunology, 2009
Circulating mannan (or mannose)-binding lectin (MBL) is genetically determined. Low MBL concentrations are associated with certain point mutations in the human MBL2 gene. Here we report the full MBL2 genotypes of 1800 Polish neonates and relate individual genotypes to serum MBL and MBL-dependent activity of the lectin pathway of complement activation. The seven acknowledged common haplotypes were found, plus the uncommon LYPD haplotype, combining to form 33 genotypes in this population. As expected, a strong correlation existed between genotypes and serum MBL or lectin pathway activity, and the latter two entities correlated strongly with each other. However, serum MBL values varied up to greater than 90-fold within genotypes. Unexpectedly, higher lectin pathway activity was found in association with the P allele relative to the Q allele. These data from a large cohort of neonates, representing an ethnically homogenous population, suggest that the current knowledge of the genetics of MBL2 is inadequate to predict serum MBL concentration and MBL-dependent lectin pathway activity in individual subjects.