BsaB, a novel adherence factor of group B Streptococcus

Area of Science:

• Microbiology
• Infectious Diseases
• Molecular Biology

Background:

• Streptococcus agalactiae (group B Streptococcus [GBS]) causes severe neonatal, maternal, and elderly infections.
• GBS colonization in healthy adults facilitates invasion and subsequent disease.
• Bacterial surface adhesins are crucial for GBS host cell and extracellular matrix attachment.

Purpose of the Study:

• To identify and characterize novel surface proteins involved in GBS adherence and colonization.
• To investigate the role of a conserved GBS surface protein in host-pathogen interactions.

Main Methods:

• Gene deletion and complementation in GBS strain 515.
• Adherence assays using VK2 vaginal and ME-180 cervical epithelial cells.
• Bacterial binding assays with fibronectin-coated microtiter wells.
• Expression of the GBS protein in Lactococcus lactis.

Main Results:

• Deletion of the GBS surface adhesin B (BsaB) gene reduced bacterial adherence to epithelial cells and fibronectin.
• Recombinant BsaB expression in L. lactis enhanced adherence to epithelial cells, fibronectin, and laminin.
• BsaB expression increased biofilm formation and its adherence function depended on the BID1 domain and C-terminal region.
• BsaB expression in GBS was regulated by the CsrRS two-component system.

Conclusions:

• BsaB is a novel GBS adhesin mediating attachment to host epithelial cells and extracellular matrix.
• BsaB plays a significant role in GBS colonization and infection processes.
• Understanding BsaB function provides potential targets for therapeutic interventions against GBS infections.