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Related Experiment Video

Updated: Nov 20, 2025

Induction of Leptomeningeal Cells Modification Via Intracisternal Injection

Induction of Leptomeningeal Cells Modification Via Intracisternal Injection

Published on: May 7, 2020

CC17 group B Streptococcus exploits integrins for neonatal meningitis development.

Romain Deshayes de Cambronne¹, Agnès Fouet¹, Amandine Picart¹

¹Université de Paris, Institut Cochin, INSERM, U1016, CNRS, UMR8104, Paris, France.

The Journal of Clinical Investigation

|January 19, 2021

Summary

Group B Streptococcus (GBS) meningitis in newborns is often caused by CC17-GBS. This study reveals CC17-GBS uses host integrins to invade the brain, offering new therapeutic targets.

Keywords:

Bacterial infections Infectious disease Integrins Microbiology

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A Murine Model of Group B Streptococcus Vaginal Colonization

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Published on: November 16, 2016

Area of Science:

Microbiology
Neuroscience
Immunology

Background:

Group B Streptococcus (GBS) is a leading cause of neonatal infections, with CC17-GBS responsible for most meningitis cases.
The mechanism by which GBS crosses the blood-brain barrier to cause meningitis is not fully understood.

Purpose of the Study:

To identify the molecular mechanisms by which CC17-GBS invades the central nervous system (CNS).
To investigate the role of host integrins in CC17-GBS meningitis and neonate susceptibility.

Main Methods:

Identified host integrin ligands for the CC17-GBS adhesin Srr2 using molecular interaction studies.
Utilized a blood-brain barrier cellular model to assess GBS adhesion and internalization.
Examined integrin expression in neonatal brain vasculature.
Tested the efficacy of integrin blocking in a mouse model of neonatal meningitis.

Main Results:

The CC17-GBS adhesin Srr2 binds to host integrins α5β1 and αvβ3 via specific motifs.
These integrins mediate GBS adhesion and internalization across the blood-brain barrier model.
Integrins α5β1 and αvβ3 are overexpressed in neonatal brain vessels and contribute to meningitis susceptibility.
Blocking these integrins reduced GBS CNS invasion in juvenile mice.

Conclusions:

CC17-GBS utilizes host integrins α5β1 and αvβ3 to facilitate CNS invasion and cause meningitis.
Integrin overexpression during the neonatal period contributes to susceptibility to GBS meningitis.
Targeting these integrins presents a potential therapeutic strategy for GBS meningitis.