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A Murine Model of Group B Streptococcus Vaginal Colonization
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Group B Streptococcus Drives Major Transcriptomic Changes in the Colonic Epithelium.

Kristen Domínguez1, April K Lindon1, Justin Gibbons1

  • 1Molecular Medicine, Morsani College of Medicine, University of South Florida, Tampa, Florida, USA.

Infection and Immunity
|June 6, 2023
PubMed
Summary

Group B Streptococcus (GBS) uses its β-hemolysin/cytolysin (βH/C) toxin to cause infant sepsis by translocating from the gut. This study shows βH/C is crucial for GBS to spread to other organs in newborns.

Keywords:
Group B Streptococcushost transcriptomeneonatal sepsistoxin

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Area of Science:

  • Microbiology
  • Neonatal Immunology
  • Pathogenesis

Background:

  • Group B Streptococcus (GBS) is a major cause of infant sepsis globally.
  • Gastrointestinal colonization precedes late-onset GBS disease in newborns.
  • Mechanisms of GBS intestinal translocation in neonates are not fully understood.

Purpose of the Study:

  • To investigate the role of GBS β-hemolysin/cytolysin (βH/C) in intestinal colonization and translocation.
  • To determine βH/C's contribution to the pathogenesis of late-onset GBS disease.

Main Methods:

  • A mouse model of late-onset GBS disease was used, exposing animals to wild-type GBS or a βH/C-deficient mutant.
  • Bacterial burden, host cell transcriptomes, and mortality were analyzed post-exposure.
  • RNA sequencing and bioinformatic analyses identified host gene expression changes.

Main Results:

  • GBS translocation to extraintestinal tissues occurred only with wild-type GBS, not the mutant.
  • Colonization led to significant transcriptomic alterations in the colon, not the small intestine.
  • βH/C was implicated in disrupting epithelial barriers and altering immune signaling.

Conclusions:

  • GBS βH/C is essential for bacterial translocation and pathogenesis of late-onset GBS disease.
  • βH/C contributes to GBS virulence by affecting host intestinal epithelial integrity and immune responses.