Activation of Toll-like receptors in meconium aspiration syndrome

J Perinatol. 2018 Feb;38(2):137-141. doi: 10.1038/jp.2017.169. Epub 2017 Nov 2.

Abstract

Objective: Meconium aspiration syndrome (MAS) is a common cause of neonatal morbidity and mortality. Incomplete understanding of the pathogenesis of MAS has hindered the development of specific therapies. We hypothesized that activation of Toll-like receptors (TLRs) might play a role in the pathogenesis of MAS. The present study evaluated the expression of TLR 1, 4, 7, 8 and 9 in neonates with MAS.

Study design: The study included 39 neonates with MAS and 17 healthy gestational age-matched neonates as controls. Neonates with maternal chorioamnionitis, perinatal asphyxia, sepsis and congenital malformations were excluded. Good-quality total RNA from umbilical cord blood was reverse transcribed to prepare cDNA using Bio-Rad reverse transcription kit. This cDNA was used to study the expression status of TLR 1, 4, 7, 8 and 9 by real-time quantitative polymerase chain reaction.

Results: Compared with controls, TLR1 and TLR4 were highly expressed, TLR9 was moderately expressed, TLR7 was weakly expressed and TLR8 expression was neutral in neonates with MAS. Within the MAS group, no difference in TLR expression was observed with respect to consistency of meconium, severity of the disease, oxygenation index and outcome.

Conclusion: There is activation of TLRs in neonates with MAS. We speculate that these TLRs probably act as endogenous ligands for various components of meconium that initiate the inflammatory cascade of MAS and contribute to its pathogenesis.

Publication types

  • Observational Study

MeSH terms

  • Biomarkers / blood
  • Case-Control Studies
  • Female
  • Fetal Blood
  • Gestational Age
  • Humans
  • Infant, Newborn
  • Inflammation / metabolism*
  • Male
  • Meconium Aspiration Syndrome / blood
  • Meconium Aspiration Syndrome / metabolism*
  • Prospective Studies
  • Signal Transduction
  • Toll-Like Receptors / blood
  • Toll-Like Receptors / metabolism*

Substances

  • Biomarkers
  • Toll-Like Receptors