Abstract |
Histological chorioamnionitis (HCA) is an established marker of ascending infection, a major cause of preterm birth. No studies have characterised the global change in expression of genes involved in the toll-like receptor (TLR) signalling pathways in the presence of HCA in the setting of preterm birth ( pHCA). Fetal membranes were collected immediately after delivery and underwent histological staging for inflammation to derive 3 groups; term spontaneous labour without HCA (n = 9), preterm birth <34 weeks gestation without HCA (n = 8) and pHCA <34 weeks (n = 12). Profiling arrays ran in triplicate for each group were used to determine the expression of 84 genes associated with TLR signalling and screen for genes of interest (fold change >2; p<0.1). Expression of identified genes was validated individually for all samples, relative to GAPDH, using RT-PCR. Expression of TLR 1, TLR 2, lymphocyte antigen 96, interleukin 8 and Interleukin-1 receptor-associated kinase-like 2 was increased in pHCA (p<0.05). Degree of expression was positively associated with histological staging of both maternal and fetal inflammation (p<0.05). The inflammatory expression profile at the maternal/fetal interface associated with pHCA, a reflection of ascending infection, is extremely heterogeneous suggesting polymicrobial involvement with activation of a common pathway. Antagonism of TLR 1 and TLR 2 signalling in this setting warrants further assessment.
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Authors | Gareth J Waring, Stephen C Robson, Judith N Bulmer, Alison J Tyson-Capper |
Journal | PloS one
(PLoS One)
Vol. 10
Issue 5
Pg. e0124298
( 2015)
ISSN: 1932-6203 [Electronic] United States |
PMID | 25965269
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- TLR2 protein, human
- Toll-Like Receptor 1
- Toll-Like Receptor 2
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Topics |
- Adult
- Amnion
(metabolism)
- Chorioamnionitis
(diagnosis, metabolism)
- Female
- Humans
- Pregnancy
- Premature Birth
(diagnosis, metabolism)
- Signal Transduction
- Toll-Like Receptor 1
(genetics, metabolism)
- Toll-Like Receptor 2
(genetics, metabolism)
- Up-Regulation
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