Fetal membrane bacterial load is increased in histologically confirmed inflammatory chorioamnionitis: A retrospective

Rochelle Hockney1, Gareth J Waring2, Gillian Taylor1

  • 1School of Health and Life Sciences, Teesside University, Middlesbrough, TS1 3BX, UK; National Horizons Centre, Teesside University, 38 John Dixon Lane, Darlington, DL1 1HG, UK.

Placenta
|March 17, 2020
PubMed
Abstract

Insights

Increased bacterial load in fetal membranes correlates with histological chorioamnionitis (HCA) severity and inflammatory markers. This suggests infection drives HCA inflammation in a dose-dependent manner.

Area of Science:

  • Obstetrics and Gynecology
  • Microbiology
  • Immunology

Background:

  • The presence and role of a fetal membrane microbiome are debated.
  • Chorioamnionitis (HCA) is a key cause of preterm birth, characterized by fetal membrane inflammation.
  • The link between bacterial load and HCA severity requires further elucidation.

Purpose of the Study:

  • To investigate the correlation between bacterial load in fetal membranes and histological chorioamnionitis (HCA).
  • To assess the relationship between bacterial load, histological staging, and inflammatory markers in HCA.

Main Methods:

  • Fetal membrane samples from HCA, preterm, and term labor groups were analyzed.
  • Bacterial 16S rRNA gene sequencing determined microbial profiles.
  • Quantitative PCR (qPCR) measured bacterial load (copy number/mg tissue).

Main Results:

  • Significantly higher bacterial load in HCA amnion and chorion compared to controls.
  • Positive correlation between bacterial load and HCA histological staging (p=0.001).
  • Increased bacterial load associated with elevated inflammatory markers (IL8, TLR1, TLR2, LY96, IRAK2).

Conclusions:

  • Histological chorioamnionitis (HCA) is linked to infection and increased bacterial load.
  • Bacterial load demonstrates a dose-response relationship with HCA severity and TLR pathway activation.
  • Further studies needed to define bacterial load thresholds triggering HCA inflammation.