Role of Toll-like receptor 4 in inflammation-induced preterm delivery.

The aim of the present study was to investigate the potential role of Toll-like receptor 4 (TLR4) in lipopolysaccharide (LPS)-induced preterm delivery. Intraperitoneal injection of LPS in the presence or absence of previous TLR4 blockade was performed to establish a murine model of preterm delivery. The incidences of preterm delivery and fetal death were calculated. Flow cytometry was performed to examine the percentages of blood CD45(+)CD86(+), CD3(+)CD69(+), CD19(+)CD69(+) and CD49b(+)CD69(+) cell subsets, and the percentages of placenta CD45(+)CD86(+), CD45(+)CD49b(+) and CD49b(+)CD69(+) cell subpopulations. In our study, an inflammation-induced preterm delivery model was established by intraperitoneal injection of LPS. Blocking TLR4 significantly decreased LPS-induced preterm delivery and fetal death. LPS treatment markedly up-regulated the percentages of blood CD45(+)CD86(+), CD3(+)CD69(+) and CD49b(+)CD69(+) cells, and of placenta CD45(+)CD86(+), CD45(+)CD49b(+) and CD49b(+)CD69(+) cells. TLR4 blockade almost completely abrogated LPS-induced elevated cell proportions. These data demonstrate that TLR4 plays a critical role in inflammation-induced preterm delivery.