Group B Streptococcus Drives Major Transcriptomic Changes in the Colonic Epithelium.

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.