Poster Presentation The Annual Scientific Meeting of the Endocrine Society of Australia and the Society for Reproductive Biology 2014

Cord blood microRNAs that regulate TLR pathways are differentially expressed depending on gestational age. (#206)

Natalie Aboustate 1 , Nicolette Hodyl 1 , Michael Stark 1 , Vicki Clifton 1
  1. University of Adelaide, Adelaide, SA, Australia

Background: Infants born preterm are at increased risk of developing inflammatory conditions in the neonatal period. This may be due to functional differences in innate inflammatory responses between preterm and term neonates. We have previously demonstrated that stimulation of cord blood from preterm neonates with toll-like receptor (TLR) 2, TLR3 and TLR4 agonists produce higher levels of interleukin-6 (IL-6) compared to term neonates. This suggests there are gestational age differences in regulation of the innate immune response, potentially mediated by differential microRNA (miR) expression.  The expression of miRs in cord blood from preterm and term neonates has not been characterised.

Methods: Cord blood from preterm and term neonates was collected at delivery and RNA extracted using the TRIzol method. The relative expression of TLR2, TLR3 and TLR4 mRNA, as well as miRs known to regulate TLR pathways (let7e, miR155, miR146a and miR146b) was determined using qPCR. Data were analysed according to gestational age and antenatal betamethasone exposure.

Results: TLR4 mRNA expression was increased in preterm cord blood compared to term (p<0.05), while no differences in TLR2 or TLR3 mRNA were observed. Expression of let7e was significantly reduced in preterm cord blood compared to term (p<0.05), while a trend towards increased miR155 expression was observed. Expression of miR146a and miR146b was not affected by preterm birth. Betamethasone exposure had no effect on miR expression.

Conclusions: The parallel decrease in the expression of the microRNA let7e with increased TLR4 expression supports previous observations of this miRs regulatory role in the TLR4 pathway. These preliminary findings indicate that inflammatory pathways in preterm neonates may be mediated by differential miR expression compared to terms.