Group B streptococcal membrane vesicles induce proinflammatory responses in neonatal meninges.
Overview
- Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, Colorado, USA
- Department of Pediatrics, Section of Developmental Biology, University of Colorado School of Medicine, Aurora, Colorado, USA
- Department of Biological Sciences, University of Texas at Dallas, Richardson, Texas, USA
- Department of Biochemistry, Duke University Medical Center, Durham, North Carolina, USA
Abstract
Streptococcus agalactiae (Group B Streptococcus; GBS) is the leading cause of neonatal meningitis, resulting in morbidity and lasting neurological effects in survivors. GBS makes three unique glycolipids in their cell membrane, which we have previously shown to promote bloodstream survival and meningitis. GBS also produces membrane vesicles (MVs), but the lipid content is not known, nor is it known how glycolipids impact MV biogenesis, cargo, and function. Additionally, it is currently unknown how GBS MVs may contribute to systemic infection, meningitis, and resulting neuroinflammation. Here, using our isogenic lipid mutants in a clinically relevant sequence type 17 and capsule type III strain, we identify that the MV lipidome replicates that of the parent bacterial cell, and that MVs isolated from a glycolipid-devoid strain have an altered MV proteome. Investigating the impact of GBS MVs on brain endothelial cells in vitro, we observe significant increases in proinflammatory chemokines CXCL-1 and IL-6 from MVs isolated from WT and lipid mutant strains. Furthermore, we show that the proteins on the MV surface contribute to cytokine induction, which is dependent on Toll-like receptor 2 (TLR2)-mediated signaling. Finally, using a neonatal murine infection model, we observe significant increases in proinflammatory chemokines CXCL-1, IL-6, TNFα, and IL-1β in the murine leptomeninges and brain when GBS MVs are present in the cerebrospinal fluid. This work reveals unexplored functions of bacterial glycolipids in MV biogenesis and identifies GBS MVs as potent inflammatory molecules to the meninges and brain endothelium that may contribute significantly to meningitis disease progression.
Reproduced under the paper's license (CC BY), from the paper cited above.
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Data
Datasets cited
- bioproject:PRJNA1441633 — at NCBI BioProject; found in “DATA AVAILABILITY”
Data availability
RNA-seq reads are available under NCBI SRA accession number PRJNA1441633 (https://
Reproduced under the paper's license (CC BY), from the paper cited above.
Versions
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Version 1, 27 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 8 authors, 4 keywords, 12 MeSH terms, 7 funders, 53 references, 1 RRID.
Cite
This paper
Joyce, L. R., Brady, A., Kim, S., Christensen, P. M., Palmer, K. L., Guan, Z., Siegnethaler, J. A., & Doran, K. S. (2026). Group B streptococcal membrane vesicles induce proinflammatory responses in neonatal meninges. Infection and immunity, 94(7), e00231-26. https://
BibTeX
@article{joyce2026group,
author = {Joyce, Luke R and Brady, Amanda and Kim, Sol and Christensen, Priya M and Palmer, Kelli L and Guan, Ziqiang and Siegnethaler, Julie A and Doran, Kelly S},
title = {{Group B streptococcal membrane vesicles induce proinflammatory responses in neonatal meninges}},
journal = {Infection and immunity},
year = {2026},
month = jun,
volume = {94},
number = {7},
pages = {e00231--26},
publisher = {American Society for Microbiology (ASM)},
issn = {0019-9567},
doi = {10.1128/
url = {https://
pmid = {42390103},
pmcid = {PMC13367065}
}
RIS
TY - JOUR
AU - Joyce, Luke R
AU - Brady, Amanda
AU - Kim, Sol
AU - Christensen, Priya M
AU - Palmer, Kelli L
AU - Guan, Ziqiang
AU - Siegnethaler, Julie A
AU - Doran, Kelly S
TI - Group B streptococcal membrane vesicles induce proinflammatory responses in neonatal meninges
T2 - Infection and immunity
J2 - Infect Immun
PY - 2026
DA - 2026/
VL - 94
IS - 7
SP - e00231
EP - 26
SN - 0019-9567
PB - American Society for Microbiology (ASM)
DO - 10.1128/
UR - https://
LA - en
ER -
CSL-JSON
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