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Marcadores da imunomodulação no sangue materno e fetal e nas placentas de mães diabéticas ou com hiperglicemia gestacional leve

  • Hara, Cristiane de Castro Pernet
Publication Date
Dec 01, 2016
Repositório Institucional UNESP
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INTRODUCTION - During pregnancy, the immune response associated with diabetes alters the expression and the transfer of immune cells, including regulatory, immunoglobulins and the profile of cytokines in the maternal-fetal interface. OBJECTIVE - To evaluate the expression of NK cells, and the profile of cytokines in maternal blood, umbilical cord and placenta, quantify the production of antibodies, as well as, the passage of IgG and subclasses, via receptors FcRn in pregnancies complicated by diabetes or hyperglycemia. METHOD - were assessed 120 pregnant women, distributed as non-diabetic (ND; n=30), Mild Gestational Hyperglycemia (MGH; n=30), Gestational Diabetes Mellitus (GDM; n=30) and type 2 Diabetes Mellitus (DM2; N=30). The cells and cytokines were evaluated by flow cytometry. The concentrations of total IgG and subclasses were analyzed by ELISA. Placental transfer of the total and subclasses antibodies were defined in each assay by the ratio [(cord concentrations/maternal concentrations) x 100]. In the statistical analysis we used analysis of variance (ANOVA), followed by Tukey test, and Pearson's linear correlation, with p < 0.05. RESULTS - In the maternal blood from the hyperglycemic groups, the CD16+CD56− NK cells increased, whereas that of CD16+CD56+ decreased in GDM group. Cord blood from DM2 showed a higher proportion of CD16+CD56− and CD16−CD56+. The placental extravillous layer of GDM and DM2 showed an increase of CD16+CD56− cells and, irrespective of region, the proportion of CD16−CD56+ cells was higher in MGH and GDM and lower in DM-2. IL-2 was lower in maternal blood and IFN-𝛾����������������������� higher in maternal and cord blood from the GDM group. IL-17 was higher in maternal and cord blood from the DM-2 group. The placental extravillous layer of the MGH showed high levels of IL-4, IL-6, IL-10, IL- 17, and IFN-𝛾����������������������� and low levels of IL-1𝛽����������������������� and IL-8, whereas the placental villous layer contained high levels of IL-17 and IFN-𝛾�����������������������. The GDM group, irrespective of region, showed higher levels of IL-8. The DM-2 group, irrespective of region, placenta showed high levels of TNF-𝛼�����������������������, IL-17, and IFN-𝛾�����������������������. Maternal blood from DM-2 and cord blood from MGH exhibited a higher proportion of CD19+ expression by B cells. DM-2 showed a lower proportion of CD19+ cells in placenta. FcRn expression increased in cells from cord blood and placenta from MGH. Maternal blood, cord blood and placenta cells from DM-2 showed lower FcRn expression. The highest FcRn expression, irrespective of glycemic status, was observed in placenta cells. Maternal blood IgG levels were lower in DM-2, and cord blood IgG levels were higher in MGH. The highest levels of IgG4 were detected in the blood of hyperglycemic mothers. The highest IgG3 and IgG4 levels in cord blood were detected in MGH, and the lowest IgG2 and IgG3 levels in DM-2. CONCLUSIONS - Hyperglycemia produces inflammatory environment with high production of cytokines, presenting changes in expression of NK cells, FcRn in the placenta, in production and rate of transfer of IgG. The levels of cells expressing CD16+ and cytokines in maternal blood, cord blood, and placental tissue are modified in pregnancies complicated by diabetes. Maternal hyperglycemia compromised placental transfer of IgG1, IgG3 and IgG4. The results suggest that regardless of hyperglycemia degree, it decreases FcRn expression in placenta and blood cells and compromises the production and transfer of antibodies from maternal blood to newborns.

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