Toll-like receptors in the genesis of miscarriage


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Objective: to study changes in the expression of the Toll-like receptor (TLR)2 and TLR4 genes by cervical canal mucosal epitheliocyles and placental cells in pregnant women with urogenital infection. Setting: Russian State Medical University, Moscow. Subjects: 105 pregnant women (late second-to-early third trimester of pregnancy), including 30 women with physiological pregnancy, 45 pregnant women with urogenital infection, and 30 pregnant women with intrauterine infection (a control group). Methods: RNA was isolated from the cervical canal trophoblastic and mucosal cells by the acid-phenoi extraction technique. The real-time polymerase chain reaction was used to determine the level of expression of the TLR2 and TLR4 genes. Results: in the pregnant women with urogenital infection (caused by cytomegalovirus, herpes simplex virus, Ureaplasma, Chlamydia, Gardnella, or Candida), the expression of TLR2 and TLR4 was observed to be 5 and 2 times greater, respectively, than that in the control group. With intrauterine infection, the expression of the TLR4 gene significantly increased by 7 times. Hyperactivation of congenital immunity mechanisms led to premature tabor in more than 70%. Conclusion: TRL-mediated trophoblastic apoptosis is a new pathogenetic mechanism that is responsible for the impact of infection on the development of pregnancy complications. Polymorphism of the TLR genes determines the body 's response to the causative agents of virai and bacteria! infections and the possibility of realizing an intrauterine infection in the fetus and the newborn and plays an important role in the prediction of pregnancy outcomes. TLR may serve as markers of pregnancy complications and as a potential target of therapeutic interventions.

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