Background: The association of gene variants for interleukin 6 (IL-6) (rs1800796), interleukin 10 (IL-10) (rs1800896) and tumor necrosis factorα (TNFα (rs1800629) with the occurrence of spontaneous preterm birth (PTB) was investigated to determine whether these genetic variants are a risk factor. Methods: A total of 199 blood samples from pregnant women who had given birth prematurely and 200 control blood samples were analyzed to determine single nucleotide polymorphisms (SNPs) of genes for IL-6 (rs1800796), IL-10 (rs1800896) and TNFα (rs1800629). The control samples were samples from pregnant women with term delivery. The isolation of DNA was performed on mini-spin columns according to the manufacturer’s protocol. The quality and purity of the isolated DNA were tested using a Qubit 3 fluorometer. Genotyping was performed with an ABI PRISM 7500 SDS using TaqMan SNP genotyping assays. The genotypes obtained were analyzed using the 7500 Software v2.3 package. Results: Carriers of the A/A genotype for the rs1800629 SNP of the TNFα gene have a 4.81 times greater chance of late-onset PTB compared to carriers of the G/G and A/G genotypes in the recessive inheritance model. The presence of the G/G genotype in the recessive inheritance model compared with the G/A and A/A genotypes for the rs1800896 SNP of the IL-10 gene represents a potentially protective factor, with mothers in the term-birth group having an almost 2-fold lower odds of PTB in general and an almost 10-fold lower odds of early PTB. On the other hand, carriers of the A/G genotype of rs1800896 have a 1.54-fold higher chance of preterm birth in general and a 1.6-fold higher chance of late preterm birth in the superdominant inheritance model compared to the A/A and G/G genotypes in the group of mothers with PTB. In this study, no association was found between PTB and the rs1800796 SNP of the IL-6 gene. Conclusions: rs1800629 in mothers was associated with PTB. rs1800896 shows a potentially protective effect for the occurrence of PTB in this study. No association was found between PTB and rs1800796.

Preterm birth (PTB) is a leading cause of neonatal morbidity and mortality worldwide. This study investigated six single-nucleotide polymorphisms (SNPs) in the maternal and fetal progesterone receptor (PGR) gene and their association with spontaneous PTB, considering environmental and clinical risk factors. We conducted a case–control study including two groups of pregnant women (term and preterm, 292 in total) and two groups of newborns (term and preterm, 292 in total), and analyzed PGR variants (rs1042838, rs1042839, rs10895068, rs4574732, rs653752, and rs1942836) in relation to maternal age, fetal gender, and pregnancy complications such as vaginal bleeding. Results showed that PGR SNPs rs1942836 (OR 0.38, CI 95% 0.15–0.98, p = 0.03), rs4574732 (OR 2.4, CI 95% 1.01–5.57, p = 0.04), and rs653752 (OR 2.27, CI 95% 1.19–4.34, p = 0.02) were associated with PTB when considered in the context of clinical factors, highlighting gene–environment interactions. Our findings underscore the importance of integrating genetic and clinical information for a better understanding of PTB risk.

Introduction: The association of gene variants for interleukin 6(IL-6) (rs1800796), interleukin 10 (IL-10) (rs1800896) and tumor necrosis factorα (TNFα (rs1800629) with the occurrence of spontaneous preterm birth (PTB) was investigated to determine whether these genetic variants are a risk factor. Materials and methods: 199 blood samples from pregnant women who had given birth prematurely and 200 control blood samples were analyzed to determine single nucleotide polymor-phisms (SNPs) of genes for IL-6 (rs1800796), IL-10 (rs1800896) and TNFα (rs1800629). The control samples were samples from pregnant women with term delivery. Isolation of DNA was per-formed on mini-spin columns according to the manufacturer's protocol. The quality and purity of the isolated DNA were tested using a Qubit 3 fluorometer. Genotyping was performed with an ABI PRISM 7500 SDS using TaqMan SNP genotyping assays. The genotypes obtained were an-alyzed using the 7500 Software v2.3 package. Results: Carriers of the A/A genotype for the rs1800629 of the TNFα gene have 4.81 times greater chance of late-onset PTB compared to carriers of the G/G and A/G genotypes in the recessive inheritance model. The presence of the G/G genotype in the recessive inheritance model compared with the G/A and A/A genotypes for the rs1800896 of the IL-10 gene represents a potentially protective factor, with mothers in the term-birth group having an almost 2-fold lower odds of PTB in general and an almost 10-fold lower odds of early PTB. On the other hand, carriers of the A/G genotype of rs1800896 have a 1.54-fold higher chance of preterm birth in general and a 1.6-fold higher chance of late preterm birth in the super dominant inheritance model compared to the A/A and G/G genotypes in the group of mothers with PTB. In this study, no association was found between PTB and rs1800796 of the IL-6 gene. Conclusion: rs1800629 in mothers was associated with PTB. rs1800896 shows a potentially protective effect for the occurrence of PTB in this study. No association was found between PTB and rs1800796.

Gestational diabetes mellitus (GDM) is a public health problem with increasing prevalence. Analyses of metabolic and immune profiles have great potential for discovering new markers and mechanisms related to the development of GDM. We monitored 61 pregnant women during the first and third trimesters of pregnancy, including 13 pregnant women with GDM, 14 pregnant women with elevated glucose in the first trimester and 34 healthy pregnant women. A number of metabolic and immunological parameters were measured, including glucose, insulin, lipid status, fatty acids, lymphocyte profile, adiponectin, IL-6, IL-10 and TNF-a. A higher number of T-helper lymphocytes and a higher ratio of helper/cytotoxic lymphocytes was found in the control group in the first trimester of pregnancy. Pregnant women whose glucose threshold values were measured in the first trimester, but who did not develop GDM, showed a higher percentage of neutrophils and a lower percentage of lymphocytes in the third trimester. Differences in polyunsaturated fatty acids levels were observed between healthy pregnant women and those with glucose metabolism disorders in the first trimester of pregnancy. The results of this pilot study demonstrate that there are differences in the profiles of T lymphocytes, NK cells and polyunsaturated fatty acids between the examined groups of pregnant women, which can serve as a direction for future research.

Background/Objectives: Gestational diabetes (GD) is a common pregnancy complication linked to inflammation. Obesity, a major risk factor, is associated with elevated pro-inflammatory markers (TNF-α, IL-6) and reduced anti-inflammatory IL-10 and adiponectin. This study investigated the role of inflammatory factors (IL-6, TNF-α, IL-10, adiponectin) and their genetic variants (rs1800629, rs1800796, rs1800896, rs266729) in a unique four-group study design of pregnant women. Methods: We collected venous blood from 162 women in the third trimester of pregnancy. We measured IL-6, IL-10, TNF-α, and adiponectin levels and performed real-time PCR genotyping for the selected SNPs. Results: IL-6 levels were significantly higher (p < 0.001) in pregnant women with GD and additional complications. The IL-6 SNP rs1800796 heterozygous CG genotype showed a slightly increased GD risk (OR = 1.41). However, we found no significant associations between GD and TNF-α rs1800629 or IL-10 rs1800896 SNPs. The AdipoQ rs266729 homozygous CC genotype was linked to increased GD risk (p = 0.03 for superdominant model). Importantly, no significant correlations were observed between inflammatory marker levels and gene variants within any study group. Conclusions: Our findings suggest a greater inflammatory burden in GD pregnancies with additional complications. While certain IL-6 and AdipoQ variants might contribute to GD risk, the overall weak association between inflammatory markers and gene variants likely reflects the complex polygenic nature of GD, environmental factors, or the study’s sample size.