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The hypervirulent Group B Streptococcus HvgA adhesin promotes central nervous system invasion through transcellular crossing of the choroid plexus.
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- معلومة اضافية
- المصدر:
Publisher: Biomed Central Country of Publication: England NLM ID: 101553157 Publication Model: Electronic Cited Medium: Internet ISSN: 2045-8118 (Electronic) Linking ISSN: 20458118 NLM ISO Abbreviation: Fluids Barriers CNS Subsets: MEDLINE
- بيانات النشر:
Original Publication: London : Biomed Central
- الموضوع:
- نبذة مختصرة :
Background: Group B Streptococcus (GBS) is the leading cause of neonatal meningitis responsible for a substantial cause of death and disability worldwide. The vast majority of GBS neonatal meningitis cases are due to the CC17 hypervirulent clone. However, the cellular and molecular pathways involved in brain invasion by GBS CC17 isolates remain largely elusive. Here, we studied the specific interaction of the CC17 clone with the choroid plexus, the main component of the blood-cerebrospinal fluid (CSF) barrier.
Methods: The interaction of GBS CC17 or non-CC17 strains with choroid plexus cells was studied using an in vivo mouse model of meningitis and in vitro models of primary and transformed rodent choroid plexus epithelial cells (CPEC and Z310). In vivo interaction of GBS with the choroid plexus was assessed by microscopy. Bacterial invasion and cell barrier penetration were examined in vitro, as well as chemokines and cytokines in response to infection.
Results: GBS CC17 was found associated with the choroid plexus of the lateral, 3rd and 4th ventricles. Infection of choroid plexus epithelial cells revealed an efficient internalization of the bacteria into the cells with GBS CC17 displaying a greater ability to invade these cells than a non-CC17 strain. Internalization of the GBS CC17 strain involved the CC17-specific HvgA adhesin and occurred via a clathrin-dependent mechanism leading to transcellular transcytosis across the choroid plexus epithelial monolayer. CPEC infection resulted in the secretion of several chemokines, including CCL2, CCL3, CCL20, CX3CL1, and the matrix metalloproteinase MMP3, as well as immune cell infiltration.
Conclusion: Our findings reveal a GBS strain-specific ability to infect the blood-CSF barrier, which appears to be an important site of bacterial entry and an active site of immune cell trafficking in response to infection.
(© 2024. The Author(s).)
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- Grant Information:
BioSPC Université de Paris cité; ANR-17-CE15-0026-01 Agence Nationale de la Recherche; ANR-17-CE15-0026-01 Agence Nationale de la Recherche
- Contributed Indexing:
Keywords: Blood cerebro-spinal fluid barrier; CC17; Choroid plexus; Group B Streptococcus; Meningitis
- الرقم المعرف:
0 (Adhesins, Bacterial)
- الموضوع:
Date Created: 20240816 Date Completed: 20240817 Latest Revision: 20240822
- الموضوع:
20240823
- الرقم المعرف:
PMC11330020
- الرقم المعرف:
10.1186/s12987-024-00564-2
- الرقم المعرف:
39152442
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