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Bacterial Modulation of Human Fetal Membrane Toll‐like Receptor Expression
Author(s) -
Abrahams Vikki M.,
Potter Julie A.,
Bhat Geeta,
Peltier Morgan R.,
Saade George,
Me Ramkumar
Publication year - 2013
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12016
Subject(s) - fetal membrane , fetus , lipopolysaccharide , amniotic fluid , receptor , biology , toll like receptor , inflammation , downregulation and upregulation , amnion , gene expression , andrology , immunology , microbiology and biotechnology , innate immune system , pregnancy , medicine , placenta , immune system , gene , biochemistry , genetics
Problem 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 ( TLR s); however, little is known about their expression and regulation in this tissue. The objective of this study was to evaluate the expression of TLR s 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 TLR s1–10. Results Treatment of fetal membranes with M ycoplasma hominis increased expression of TLR 4, TLR 6, and TLR 8 mRNA . U reaplasma parvum upregulated TLR 8 mRNA , and P orphyromonas gingivalis significantly increased fetal membrane TLR 7 expression. In contrast, treatment with Gram‐negative E scherichia coli (and its cell wall component lipopolysaccharide) downregulated TLR 10 mRNA . No effect was detected for U reaplasma urealyticum , G ardnerella vaginalis , or Group B Streptococcus. Conclusion 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.