Bacterial Modulation of Human Fetal Membrane Toll-like Receptor Expression
Article first published online: 11 SEP 2012
© 2012 John Wiley & Sons A/S
American Journal of Reproductive Immunology
Volume 69, Issue 1, pages 33–40, January 2013
How to Cite
Bacterial modulation of human fetal membrane Toll-like receptor expression. Am J Reprod Immunol 2013; 69: 33–40, , , , , .
- Issue published online: 7 DEC 2012
- Article first published online: 11 SEP 2012
- Manuscript Accepted: 1 AUG 2012
- Manuscript Received: 18 JUL 2012
- NIH/NICHD. Grant Numbers: RO1HD049446, PO1HD054713
- NIH. Grant Number: R03HD067446
- preterm birth;
- Toll-like receptor
Preterm premature rupture of fetal membranes (pPROM) occurs in 30–40% of spontaneous preterm births (PTB) and is associated with intra-amniotic infection and inflammation. The membranes may sense and respond to microbes via Toll-like receptors (TLRs); however, little is known about their expression and regulation in this tissue. The objective of this study was to evaluate the expression of TLRs 1–10 in fetal membranes after exposure to pathogens associated with intra-amniotic infection and PTB.
Method of study
Normal human term fetal membrane explants were exposed to various bacteria. After 24 hrs, RNA was extracted and quantitative RT-PCR performed for TLRs1–10.
Treatment of fetal membranes with Mycoplasma hominis increased expression of TLR4, TLR6, and TLR8 mRNA. Ureaplasma parvum upregulated TLR8 mRNA, and Porphyromonas gingivalis significantly increased fetal membrane TLR7 expression. In contrast, treatment with Gram-negative Escherichia coli (and its cell wall component lipopolysaccharide) downregulated TLR10 mRNA. No effect was detected for Ureaplasma urealyticum, Gardnerella vaginalis, or Group B Streptococcus.
These findings demonstrate that different types of bacteria have distinct effects on fetal membrane TLR expression patterns. Moreover, these findings highlight the disparity of fetal membrane responses to infection and thus suggest heterogeneity in the mechanisms by which infection-associated pregnancy complications, such as pPROM and PTB, arise.