Phenotypic composition of umbilical blood monocytes and health status of newborns from mothers with COVID-19

Background . COVID-19 during pregnancy affects the development of inflammatory reactions in the fetus. However, data on the impact of maternal COVID-19 on the phenotypic composition of umbilical blood monocytes in newborns are insufficiently presented. The aim . To investigate the phenotypic composition of umbilical blood monocytes in newborns and assess their health status in cases of COVID-19 in the third trimester of pregnancy. Materials and methods . A comparative study was conducted involving 62 full-term newborns from mothers with COVID-19 in the third trimester of pregnancy (main group) and 30 newborns from mothers not infected with SARS-CoV-2 (control group). Expression of CD14, HLA-DR, CD206, CD32, TNFR1, TNFR2, IL17R, and TRAIL on umbilical blood monocytes was determined using flow cytometry. Results . According to the results, the number of monocytes in the umbilical blood of newborns in the main group expressing CD14, HLA-DR, and TNFR2 was reduced by 1.54, 1.41, and 2.36 times respectively (p < 0.001) compared to the control group. The expression levels of CD206, CD32, TNFR1, IL17R, and TRAIL were increased by 3.02 (p < 0.001), 1.1 (p < 0.01), 1.3 (p < 0.001), 17.68 (p < 0.001), and 3.6 times (p < 0.001), respectively. Birth weight (p = 0.021) and height (p = 0.006) at birth were lower in newborns compared to the control group. In the evaluation using the Apgar score, no differences were found between the study groups at the first minute (p = 0.170). At the fifth minute, the values were lower than in the control group (p = 0.001). Regression analysis identified a dependence of increased morbidity in newborns on the number of umbilical blood monocytes expressing TNFR1 and TRAIL. Newborns in the main group had an increased risk of developing cerebral ischemia, motor disorder syndrome, and persistent fetal circulation. Conclusion . Maternal infection in the third trimester of pregnancy caused by SARSCoV-2 leads to the development of a fetal inflammatory response, increasing the risk of neonatal complications.