Invasion and trafficking of hypervirulent group B streptococci in polarized enterocytes

Area of Science:

• Microbiology
• Cell Biology
• Infectious Diseases

Background:

• Streptococcus agalactiae (group B Streptococcus, GBS) is a common bacterium that can cause serious infections, especially in newborns and the elderly.
• The gut is a key site for GBS colonization and a potential entry point for neonatal infections, particularly from hypervirulent CC17 strains.
• Understanding GBS interaction with intestinal cells is crucial for developing new prevention strategies.

Purpose of the Study:

• To investigate the interaction between the GBS CC17 BM110 strain and polarized human enterocytes (Caco-2 cells).
• To elucidate the mechanisms and pathways by which GBS adheres to and invades intestinal epithelial cells.
• To identify potential targets for blocking GBS intestinal barrier invasion.

Main Methods:

• Utilized the Caco-2 cell line to model polarized human enterocytes.
• Examined GBS adherence and invasion through apical and basolateral surfaces.
• Investigated internalization mechanisms using endocytosis markers and actin dynamics.
• Analyzed bacterial colocalization with endocytic markers like EEA-1.

Main Results:

• GBS demonstrated adherence to and invasion of Caco-2 cells via both apical and basolateral surfaces.
• Basolateral invasion was significantly more efficient than apical invasion, especially when cell junctions were weakened.
• Bacterial internalization involved caveolae- and lipid raft-dependent endocytosis and actin reorganization, excluding clathrin-dependent pathways.
• GBS initially colocalized with EEA-1 and subsequently resided in acidic vacuoles within host cells.

Conclusions:

• CC17 GBS preferentially adheres to and invades enterocytes through their lateral surfaces.
• The invasion mechanism relies on caveolar lipid rafts and actin-dependent endocytosis.
• These findings provide insights into GBS intestinal barrier invasion and suggest potential targets for preventive strategies.