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

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

Author information

1
Department of Obstetrics and Gynecology, Guangzhou Medical College Affiliated Guangzhou First Municipal People's Hospital, Guangzhou 510180, China. selinalee@tom.com

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.

PMID:
19995880
DOI:
10.1093/molehr/gap106
[Indexed for MEDLINE]

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