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Modeling Ascending Vaginal Infection, Preterm Birth, and Neonatal Morbidity in Mice
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Modeling Ascending Vaginal Infection, Preterm Birth, and Neonatal Morbidity in Mice

Published on: October 10, 2025

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Perinatal hormones favor CC17 group B Streptococcus intestinal translocation through M cells and hypervirulence in

Constantin Hays1,2,3,4, Gérald Touak1,2,3, Abdelouhab Bouaboud1,2,3

  • 1Institut Cochin, Team Bacteria and Perinatality, INSERM U1016, Paris, France.

Elife
|November 12, 2019
PubMed

Insights

Hormones like estradiol and progesterone at levels found in 7-day-old infants promote Group B Streptococcus (GBS) meningitis. This occurs as hormones enhance CC17 GBS clone invasion through the neonatal gut.

Area of Science:

  • Neonatal immunology
  • Microbial pathogenesis
  • Endocrinology

Background:

  • Group B Streptococcus (GBS) is a major cause of neonatal invasive bacterial infections.
  • Late-onset disease (LOD) is primarily caused by the hypervirulent CC17 GBS clone.
  • Pregnancy hormones, estradiol (E2) and progesterone (P4), are present in newborns.

Purpose of the Study:

  • To investigate the impact of neonatal hormone levels (E2-P4 C0 and C7) on GBS neonatal infection.
  • To understand the mechanisms by which CC17 GBS causes LOD.

Main Methods:

  • Utilized cellular and mouse models with hormonal exposure mimicking concentrations at birth (C0) and 7 days old (C7).
  • Infected mice orally with GBS isolates, including the CC17 clone.
  • Examined GBS translocation across the intestinal barrier via M cells.

Main Results:

  • E2-P4 C7 concentrations specifically promoted CC17 GBS meningitis in orally infected mice.
  • CC17 GBS utilizes M cells to cross the intestinal barrier.
  • The CC17-specific surface protein Srr2 mediates this translocation, enhanced by E2-P4 C7, which promotes M cell differentiation and bacterial invasiveness.

Conclusions:

  • Neonatal hormonal milieu, particularly at levels seen in 7-day-old infants, favors CC17 GBS meningitis.
  • Hormonal imprint on neonatal gastrointestinal tract maturation explains CC17 GBS's role in LOD.
  • This provides a mechanistic link between hormonal exposure and GBS pathogenesis in neonates.

Keywords:
CC17 cloneM cellsStreptococcus agalactiaeinfectious diseaseintestinal barriermicrobiologyneonatal infectionsex hormones

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