Vitamin D deficiency as a trigger of inflammation and preterm birth

Abstract

Preterm birth remains one of the leading causes of perinatal mortality and long-term morbidity in newborns. The purposeof this study was to determine the role of vitamin D deficiency in the regulation of the NF-κB-dependent pro-inflammatory cascade in pregnant women with preterm birth. Clinical, biochemical, and immunological methods were applied, including the assessment of serum 25(OH)D levels, placental p65 NF-κB activity and phosphorylated forms, and concentrations of TNF-α, IL-6, and CRP. A total of 114 pregnant women were examined and divided into three groups: preterm birth with vitamin D deficiency (n = 44), preterm birth with optimal vitamin D levels (n = 40), and a control group with physiological pregnancy (n = 30). It was established that p65 NF-κB activity was the highest in the vitamin D-deficient group – 59.21 ± 0.24%, significantly higher compared to the group with optimal vitamin D levels (47.15 ± 0.36%) and the control (28.46 ± 0.37%) (P < 0.05). TNF-α concentrations were 42.75 ± 0.31, 30.44 ± 0.29, and 15.62 ± 0.18 pg/mL, IL-6 – 38.16 ± 0.28, 26.87 ± 0.26, and 12.44 ± 0.14 pg/mL, and CRP – 6.82 ± 0.12, 4.31 ± 0.09, and 1.95 ± 0.06 mg/L, respectively (P < 0.05). Strong correlations were confirmed between NF-κB activity and TNF-α (r = 0.88), IL-6 (r = 0.85), and CRP (r = 0.79). It was summarised that vitamin D deficiency was associated with NF-κB hyperactivation and enhanced production of pro-inflammatory cytokines, contributing to preterm birth development. The obtained results may be applied in obstetric and gynecological practice for risk stratification of preterm birth and for the development of individualised preventive strategies aimed at correcting vitamin D status

Received: 09.08.2023 | Revised: 23.10.2023 | Accepted: 30.05.2023