Background: Contracting COVID-19 during pregnancy can harm both the mother and the unborn child. Pregnant women are highly likely to develop respiratory viral infection complications with critical conditions caused by physiological changes in the immune and cardiopulmonary systems. Asymptomatic COVID-19 in pregnant women may be accompanied by fetal inflammatory response syndrome, which has adverse consequences for the newborn’s life and health. Purpose: To conduct an inflammatory response assessment of the fetus due to the effects of COVID-19 on the mother during pregnancy by determining pro-inflammatory cytokines, cell markers, T regulatory cells, T cell response, evaluation of cardiac function, and thymus size. Materials and methods: A prospective study included pregnant women (n = 92). The main group consisted of 62 pregnant women with COVID-19 infection: subgroup 1—SARS-CoV-2 PCR-positive pregnant women 4–6 weeks before delivery (n = 30); subgroup 2—SARS-CoV-2 PCR-positive earlier during pregnancy (n = 32). The control group consisted of 30 healthy pregnant women. In all pregnant women, the levels of circulating cytokines and chemokines (IL-1α, IL-6, IL-8, IL-10, GM-CSF, TNF-α, IFN-γ, MIP-1β, and CXCL-10) were determined in the peripheral blood and after delivery in the umbilical cord blood, and an analysis was performed of the cell markers on dendritic cells, quantitative and functional characteristics of T regulatory cells, and specific T cell responses. The levels of thyroxine and thyroid-stimulating hormone were determined in the newborns of the studied groups, and ultrasound examinations of the thymus and echocardiography of the heart were also performed. Results: The cord blood dendritic cells of newborns born to mothers who suffered from COVID-19 4–6 weeks before delivery (subgroup 1) showed a significant increase in CD80 and CD86 expression compared to the control group (p = 0.023). In the umbilical cord blood samples of children whose mothers tested positive for COVID-19 4–6 weeks before delivery (subgroup 1), the CD4+CCR7+ T cells increased with a concomitant decrease in the proportion of naive CD4+ T cells compared with the control group (p = 0.016). Significantly higher levels of pro-inflammatory cytokines and chemokines were detected in the newborns of subgroup 1 compared to the control group. In the newborns of subgroup 1, the functional activity of T regulatory cells was suppressed, compared with the newborns of the control group (p < 0.001). In all pregnant women with a severe coronavirus infection, a weak T cell response was detected in them as well as in their newborns. In newborns whose mothers suffered a coronavirus infection, a decrease in thymus size, transient hypothyroxinemia, and changes in functional parameters according to echocardiography were revealed compared with the newborns of the control group. Conclusions: Fetal inflammatory response syndrome can occur in infants whose mothers suffered from a COVID-19 infection during pregnancy and is characterized by the activation of the fetal immune system and increased production of pro-inflammatory cytokines. The disease severity in a pregnant woman does not correlate with SIRS severity in the neonatal period. It can vary from minimal laboratory parameter changes to the development of complications in the organs and systems of the fetus and newborn.

The objective. To study neutrophil Fc-gamma receptor expression and the possibility of its modulation in premature newborns with bacterial infection. Patients and methods. We examined samples of umbilical blood and also peripheral venous blood of newborns collected on the 28-30th day of life. The method of flow cytometry was used to detect the level of surface expression of neutrophil Fc-gamma receptors (CD64, CD32, CD16), phagocytic activity and oxidative burst of granulocytes stimulated by fluorescent labelled Escherichia coli. Results. Blood samples of 48 children were examined, of them 10 - full-term newborns (group 1), 18 - premature newborns with ELBW and VLBW (group 2), 20 - premature newborns with LBW (group 3). CD64 expression at birth in premature children from the 2nd and 3rd groups was 7.1 MFI (5.1; 11.5) and 6.0 MFI (5.3; 9.8), respectively, which is significantly higher (p = 0.013) than in children from group 1 (4.27 MFI (2.4; 5.8)). CD16 expression at birth was lower (p = 0.021) in premature children (group 2: 80.9 MFI (58.7; 114.8); group 3: 99.7 MFI (71.3; 126.0)) as compared with full-term newborns (125.3 MFI (95.5; 144.1)) and increased by the end of the 1st month of life (group 2: 118.5 MFI (99.5; 132.2); group 3: 126.6 MFI (110.1; 129.0)). Analysis of CD32 expression did not show statistically significant differences in the groups of study. A correlation between the intensity of oxidative burst of neutrophils and gestational age has been shown (Rs = 0.67; p = 0.0005). Granulocyte cultivation in the presence of G-CSF brings about a 2.4-5-fold increase of CD16, CD32 expression and enhanced oxidative burst. Conclusion. Premature newborns are characterised by dysregulation of Fc-gamma receptor expression and functional deficiency of neutrophils. G-CSF modulates CD16 and CD32 expression on the neutrophil surface and enhances oxidative burst.