Role of Inflammatory Mediators in Endothelial Dysfunction of Umbilical Cord Vessels in Pregnant Women after Third-Trimester Nonprimary Cytomegaloviral Infection

Background. Endothelial cells are the site of productive replication, hematogenous spread and persistence for a variety of viruses, including cytomegalovirus, which play a critical role in the development of vascular complications associated with cytomegalovirus infection due to developing endothelial dysfunction.Aim: to reveal the role of inflammatory mediators (tumor necrosis factor alpha, interleukin-1β, interleukin-8) in the formation of umbilical cord vascular endothelial dysfunction in reactivation of latent cytomegalovirus infection in the third trimester of pregnancy.Material and methods. The standard method of solid-phase (“sandwich” variant) enzyme immunoassay was carried out to study pro-inflammatory cytokines (tumor necrosis factor alpha, interleukin-1β, -8), endothelin-1, nitrite anion in the blood of the umbilical cord of newborns from mothers who come through reactivation of latent cytomegalovirus infection in the third trimester of pregnancy. The work includes examination data of 78 newborns born at 38–40 weeks of gestation. Among them: 45 newborns were born by CMV-seropositive women with reactivation of latent cytomegalovirus infection in the third trimester of pregnancy (main group) and 33 – by CMV-seronegative women (control group). Umbilical vein blood serum was chosen as the material for the study.Results. In the blood of the umbilical vein of newborns from mothers with reactivation of latent cytomegalovirus infection in the third trimester of pregnancy, a high level of pro-inflammatory cytokines was detected: tumor necrosis factor alpha, interleukin-1β, interleukin-8 (p < 0.001) with a simultaneous increase in the content of endothelin-1 and nitrite anion (p < 0.001), compared with similar indicators for healthy newborns.Conclusion. Reactivation of latent cytomegalovirus infection in the third trimester of pregnancy is associated with the formation of a systemic fetal inflammatory response determined by a high concentration of inflammatory mediators (tumor necrosis factor alpha, interleukin-1β, interleukin-8) and an increase in vasoactive compounds (endothelin-1 and nitrite-anion) leading to the formation of dysfunction of the vascular endothelium of the umbilical cord.