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

Mol Hum Reprod. 2010 Apr;16(4):267-72. doi: 10.1093/molehr/gap106. Epub 2009 Dec 7.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • B-Lymphocytes / drug effects
  • B-Lymphocytes / immunology
  • B7-2 Antigen / metabolism
  • Female
  • Flow Cytometry
  • Killer Cells, Natural / drug effects
  • Killer Cells, Natural / immunology
  • Leukocytes / drug effects
  • Leukocytes / metabolism
  • Lipopolysaccharides* / toxicity
  • Lymphocyte Activation / drug effects
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Pregnancy
  • Premature Birth / chemically induced*
  • Premature Birth / immunology*
  • Premature Birth / metabolism
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / immunology
  • Toll-Like Receptor 4 / antagonists & inhibitors*
  • Toll-Like Receptor 4 / metabolism*

Substances

  • B7-2 Antigen
  • Lipopolysaccharides
  • Toll-Like Receptor 4