Features of cytokine profile in the “Mother – Preterm newborn” system

Abstract

Relevance: Preterm birth remains one of the leading causes of perinatal morbidity and mortality. Disruption of the immune balance toward Th1-oriented hyperactivation and insufficient anti-inflammatory regulation (particularly IL-10) contributes to cytokine cascade activation, placental barrier injury, and the initiation of preterm labor. Cytokines and their receptors (IL-2, IL-10, TNF-α, CD210, CD212) play a key role in maternal–fetal immunological interactions, yet coordinated immune changes in the mother–infant system remain insufficiently studied.

The study aimed to evaluate the immunological profile of mothers and their preterm newborns and to identify immune correlations within the “mother – preterm newborn” system that reflect the pathogenesis of immune changes associated with preterm birth.

Materials and Methods: A cohort study included 200 women with spontaneous preterm delivery at 22–36 weeks of gestation and their newborns. Maternal and neonatal levels of TNF-α, IL-2, IL-10, and expression of CD210, CD212, CD95, and CD25 on T-lymphocytes and monocytes were assessed. Clinical outcomes included necrotizing enterocolitis, bronchopulmonary dysplasia, intraventricular hemorrhage, invasive mechanical ventilation, pneumonia, and mortality.

Results: Correlation analysis revealed significant associations between maternal cytokine levels (IL-2, IL-10, TNF-α), the expression of CD210 and CD212 receptors, and corresponding parameters in newborns (q < 0.05), indicating coordinated pro-inflammatory and anti-inflammatory mechanisms within the “mother – fetus” system. In newborns, increased T-cell and cytokine activity was associated with a higher risk of infectious and inflammatory complications. An immune risk profile was identified, characterized by elevated TNF-α, IL-2, CD212⁺ , and CD95⁺ levels, and decreased IL-10 and CD25⁺ expression.

Conclusions: Mothers and preterm newborns show tightly interconnected immune profiles, confirming coordinated immune responses within the maternal-fetal system. A shift toward a pronounced pro-inflammatory Th1-dominant pattern, combined with reduced regulatory capacity, is associated with NEC, IMV dependence, IVH, and mortality. Key immune markers – IL-2, IL-10, TNF-α, CD95, CD210, and CD212 – may serve as predictors of adverse neonatal outcomes, supporting early risk stratification and the development of personalized immunomodulatory approaches.