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

Group B Streptococcus (GBS) is the leading cause of invasive bacterial neonatal infections. Late-onset diseases (LOD) occur between 7 and 89 days of life and are largely due to the CC17 GBS hypervirulent clone. We studied the impact of estradiol (E2) and progesterone (P4), which impregnate the fetus...

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Main Authors: Constantin Hays, Gérald Touak, Abdelouhab Bouaboud, Agnès Fouet, Julie Guignot, Claire Poyart, Asmaa Tazi
Format: Article
Language:English
Published: eLife Sciences Publications Ltd 2019-11-01
Series:eLife
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Online Access:https://elifesciences.org/articles/48772
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author Constantin Hays
Gérald Touak
Abdelouhab Bouaboud
Agnès Fouet
Julie Guignot
Claire Poyart
Asmaa Tazi
author_facet Constantin Hays
Gérald Touak
Abdelouhab Bouaboud
Agnès Fouet
Julie Guignot
Claire Poyart
Asmaa Tazi
author_sort Constantin Hays
collection DOAJ
description Group B Streptococcus (GBS) is the leading cause of invasive bacterial neonatal infections. Late-onset diseases (LOD) occur between 7 and 89 days of life and are largely due to the CC17 GBS hypervirulent clone. We studied the impact of estradiol (E2) and progesterone (P4), which impregnate the fetus during pregnancy, on GBS neonatal infection in cellular and mouse models of hormonal exposure corresponding to concentrations found at birth (E2-P4 C0) and over 7 days old (E2-P4 C7). Using representative GBS isolates, we show that E2-P4 C7 concentrations specifically favor CC17 GBS meningitis following mice oral infection. CC17 GBS crosses the intestinal barrier through M cells. This process mediated by the CC17-specific surface protein Srr2 is enhanced by E2-P4 C7 concentrations which promote M cell differentiation and CC17 GBS invasiveness. Our findings provide an explanation for CC17 GBS responsibility in LOD in link with neonatal gastrointestinal tract maturation and hormonal imprint.
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spelling doaj.art-48f913a41b0e4becbca0b66a033487082022-12-22T02:01:18ZengeLife Sciences Publications LtdeLife2050-084X2019-11-01810.7554/eLife.48772Perinatal hormones favor CC17 group B Streptococcus intestinal translocation through M cells and hypervirulence in neonatesConstantin Hays0Gérald Touak1Abdelouhab Bouaboud2Agnès Fouet3Julie Guignot4Claire Poyart5Asmaa Tazi6https://orcid.org/0000-0001-9531-9177Institut Cochin, Team Bacteria and Perinatality, INSERM U1016, Paris, France; CNRS UMR 8104, Paris, France; Paris Descartes University, Paris, France; Department of Bacteriology, University Hospitals Paris Centre-Cochin, Assistance Publique – Hôpitaux de Paris, Paris, FranceInstitut Cochin, Team Bacteria and Perinatality, INSERM U1016, Paris, France; CNRS UMR 8104, Paris, France; Paris Descartes University, Paris, FranceInstitut Cochin, Team Bacteria and Perinatality, INSERM U1016, Paris, France; CNRS UMR 8104, Paris, France; Paris Descartes University, Paris, FranceInstitut Cochin, Team Bacteria and Perinatality, INSERM U1016, Paris, France; CNRS UMR 8104, Paris, France; Paris Descartes University, Paris, FranceInstitut Cochin, Team Bacteria and Perinatality, INSERM U1016, Paris, France; CNRS UMR 8104, Paris, France; Paris Descartes University, Paris, FranceInstitut Cochin, Team Bacteria and Perinatality, INSERM U1016, Paris, France; CNRS UMR 8104, Paris, France; Paris Descartes University, Paris, France; Department of Bacteriology, University Hospitals Paris Centre-Cochin, Assistance Publique – Hôpitaux de Paris, Paris, France; National Reference Center for Streptococci, Paris, FranceInstitut Cochin, Team Bacteria and Perinatality, INSERM U1016, Paris, France; CNRS UMR 8104, Paris, France; Paris Descartes University, Paris, France; Department of Bacteriology, University Hospitals Paris Centre-Cochin, Assistance Publique – Hôpitaux de Paris, Paris, France; National Reference Center for Streptococci, Paris, FranceGroup B Streptococcus (GBS) is the leading cause of invasive bacterial neonatal infections. Late-onset diseases (LOD) occur between 7 and 89 days of life and are largely due to the CC17 GBS hypervirulent clone. We studied the impact of estradiol (E2) and progesterone (P4), which impregnate the fetus during pregnancy, on GBS neonatal infection in cellular and mouse models of hormonal exposure corresponding to concentrations found at birth (E2-P4 C0) and over 7 days old (E2-P4 C7). Using representative GBS isolates, we show that E2-P4 C7 concentrations specifically favor CC17 GBS meningitis following mice oral infection. CC17 GBS crosses the intestinal barrier through M cells. This process mediated by the CC17-specific surface protein Srr2 is enhanced by E2-P4 C7 concentrations which promote M cell differentiation and CC17 GBS invasiveness. Our findings provide an explanation for CC17 GBS responsibility in LOD in link with neonatal gastrointestinal tract maturation and hormonal imprint.https://elifesciences.org/articles/48772Streptococcus agalactiaeCC17 cloneintestinal barrierneonatal infectionsex hormonesM cells
spellingShingle Constantin Hays
Gérald Touak
Abdelouhab Bouaboud
Agnès Fouet
Julie Guignot
Claire Poyart
Asmaa Tazi
Perinatal hormones favor CC17 group B Streptococcus intestinal translocation through M cells and hypervirulence in neonates
eLife
Streptococcus agalactiae
CC17 clone
intestinal barrier
neonatal infection
sex hormones
M cells
title Perinatal hormones favor CC17 group B Streptococcus intestinal translocation through M cells and hypervirulence in neonates
title_full Perinatal hormones favor CC17 group B Streptococcus intestinal translocation through M cells and hypervirulence in neonates
title_fullStr Perinatal hormones favor CC17 group B Streptococcus intestinal translocation through M cells and hypervirulence in neonates
title_full_unstemmed Perinatal hormones favor CC17 group B Streptococcus intestinal translocation through M cells and hypervirulence in neonates
title_short Perinatal hormones favor CC17 group B Streptococcus intestinal translocation through M cells and hypervirulence in neonates
title_sort perinatal hormones favor cc17 group b streptococcus intestinal translocation through m cells and hypervirulence in neonates
topic Streptococcus agalactiae
CC17 clone
intestinal barrier
neonatal infection
sex hormones
M cells
url https://elifesciences.org/articles/48772
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