Group B Streptococcus pili mediate adherence to salivary glycoproteins

Jane L Brittan1, Angela H Nobbs1

  • 1School of Oral & Dental Sciences, University of Bristol, Lower Maudlin Street, Bristol, BS1 2LY, UK.

Microbes and Infection
|January 11, 2015
PubMed

Insights

Group B Streptococcus (GBS) pili, specifically PI-1 and PI-2a, bind to glycoprotein-340 in human saliva. This interaction aids GBS colonization of the oropharynx, potentially leading to severe infections like sepsis and meningitis.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Molecular Biology

Background:

  • Group B Streptococcus (GBS) is a primary cause of neonatal infections and a growing threat to adults.
  • GBS colonization is the initial step for all GBS-related diseases, with the oropharynx being a common site.
  • Mechanisms of GBS colonization in the oropharynx remain poorly understood.

Purpose of the Study:

  • To investigate the mechanisms by which GBS colonizes the human oropharynx.
  • To determine the role of GBS pili in adherence to salivary components.
  • To identify specific GBS pilus types involved in binding to salivary pellicle.

Main Methods:

  • Adherence assays of GBS strains to human salivary pellicle.
  • Heterologous expression of GBS pilus island (PI) genes in Lactococcus lactis.
  • Analysis of GBS PI-2a, PI-1, and PI-2b pili binding to glycoprotein-340 (gp340).
  • Investigation of GBS aggregation by fluid-phase and immobilized gp340.

Main Results:

  • Three GBS strains demonstrated adherence to human salivary pellicle.
  • GBS PI-2a and PI-1 pili, but not PI-2b pili, bound to immobilized gp340.
  • Variations in pilus backbone and ancillary protein subunits influenced gp340 binding.
  • GBS strains aggregated by fluid-phase gp340, but this was not mediated by pili.

Conclusions:

  • GBS pili (PI-1 and PI-2a) facilitate colonization of the oropharynx by binding to gp340 in salivary pellicle.
  • Pilus-mediated adherence to immobilized gp340 may be crucial for GBS tissue colonization.
  • This mechanism allows GBS to evade innate mucosal defenses, potentially increasing the risk of invasive diseases like meningitis and sepsis.

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