Amniotic fluid NF-kB concentration in pregnant women with a high risk of prenatal screening test results
Abstract
Objectives: Nuclear factor-kappa beta (NF-kB) can potentially be related to certain fetal chromosomal abnormalities. This study aimed to determine whether the concentration of NF-kB changes in the amniotic fluid (AF) of pregnant women who have a high risk of fetal down syndrome (DS) results in prenatal screening and diagnosis testing.
Material and methods: 108 patients with an abnormal first trimester combined screening test (FTCST) were subjected to amniocentesis and fetal karyotype analysis between 16 and 20 weeks of gestation. Amniocentesis material obtained from 86 patients conformed with our research criteria and only this was included in the study. Among the 86 amniocentesis results, there were 12 patients with confirmed DS. The karyotypes of the remaining patients were normal. Therefore the total study group was divided into two groups: patients with DS fetal karyotype (Group 1, n = 12) and patients with normal fetal karyotype (Group 2, n = 74). We used the ELISA method to assess the concentration of NF-kB and high sensitivity C-reactive protein (hsCRP) in each sample of AF.
Results: We observed significantly lower NF-kB concentrations in the AF of the women in Group 1 compared with the women in Group 2. Patients in Group 1 also had a higher concentration of hsCRP in their AF when compared with patients in Group 2. The FTCST results for patients in Group 1 showed a significantly higher risk than for those of Group 2. There were no statistically significant correlations detected when comparing the amniotic fluid nuclear factor-kappa beta (AF-NF-kB) levels with other clinical and laboratory parameters.
Conclusions: AF-NF-kB may play a role in the pathogenesis of fetal down syndrome.
Keywords: down syndromenuclear factor-kappa betaamniotic fluidprenatal screening test
References
- BROMAGE S, LANG A, ATKINSON I, et al. Abnormal TGFbeta Levels in the Amniotic Fluid of Down Syndrome Pregnancies. American Journal of Reproductive Immunology. 2000; 44(4): 205–210.
- Vesce F, Scapoli C, Giovannini G, et al. Cytokine imbalance in pregnancies with fetal chromosomal abnormalities. Human Reproduction. 2002; 17(3): 803–808.
- Costa V, Sommese L, Casamassimi A, et al. Impairment of circulating endothelial progenitors in Down syndrome. BMC Medical Genomics. 2010; 3(1).
- Tak P, Firestein G. NF-κB: a key role in inflammatory diseases. Journal of Clinical Investigation. 2001; 107(1): 7–11.
- Ghosh S, Karin M. Missing Pieces in the NF-κB Puzzle. Cell. 2002; 109(2): S81–S96.
- Baldwin A. THE NF-κB AND IκB PROTEINS: New Discoveries and Insights. Annual Review of Immunology. 1996; 14(1): 649–681.
- Pahl H. Activators and target genes of Rel/NF-κB transcription factors. Oncogene. 1999; 18(49): 6853–6866.
- Gerondakis S, Grumont R, Rourke I, et al. The regulation and roles of Rel/NF-κB transcription factors during lymphocyte activation. Current Opinion in Immunology. 1998; 10(3): 353–359.
- Zbucka-Kretowska M, Charkiewicz K, Czerniecki J, et al. Amniotic Fluid Angiogenic and Inflammatory Factor Profiling in Foetal Down Syndrome. Fetal Diagnosis and Therapy. 2017; 44(1): 44–50.
- Laudanski P, Zbucka-Kretowska M, Charkiewicz K, et al. Maternal Plasma and Amniotic Fluid Chemokines Screening in Fetal Down Syndrome. Mediators of Inflammation. 2014; 2014: 1–10.
- Barkett M, Gilmore T. Control of apoptosis by Rel/NF-κB transcription factors. Oncogene. 1999; 18(49): 6910–6924.
- Wang C. NF-B Antiapoptosis: Induction of TRAF1 and TRAF2 and c-IAP1 and c-IAP2 to Suppress Caspase-8 Activation. Science. 1998; 281(5383): 1680–1683.
