Streptococcal Adhesin P (SadP) contributes to Streptococcus suis adhesion to the human intestinal epithelium

PLoS One. 2017 Apr 13;12(4):e0175639. doi: 10.1371/journal.pone.0175639. eCollection 2017.

Abstract

Background: Streptococcus suis is a zoonotic pathogen, causing meningitis and septicemia. We previously demonstrated that the gastrointestinal tract (GIT) is an entry site for zoonotic S. suis infection. Here we studied the contribution of Streptococcal adhesin Protein (SadP) to host-pathogen interaction at GIT level.

Methods: SadP expression in presence of Intestinal Epithelial Cells (IEC) was compared with expression of other virulence factors by measuring transcript levels using quantitative Real Time PCR (qRT-PCR). SadP variants were identified by phylogenetic analysis of complete DNA sequences. The interaction of SadP knockout and complementation mutants with IEC was tested in vitro.

Results: Expression of sadP was significantly increased in presence of IEC. Sequence analysis of 116 invasive strains revealed five SadP sequence variants, correlating with genotype. SadP1, present in zoonotic isolates of clonal complex 1, contributed to binding to both human and porcine IEC and translocation across human IEC. Antibodies against the globotriaosylceramide Gb3/CD77 receptor significantly inhibited adhesion to human IEC.

Conclusion: SadP is involved in the host-pathogen interaction in the GIT. Differences between SadP variants may determine different affinities to the Gb3/CD77 host-receptor, contributing to variation in adhesion capacity to host IEC and thus to S. suis zoonotic potential.

MeSH terms

  • Adhesins, Bacterial / genetics*
  • Adhesins, Bacterial / metabolism*
  • Animals
  • Bacterial Adhesion
  • Caco-2 Cells
  • Cell Line
  • Coculture Techniques
  • Host-Pathogen Interactions
  • Humans
  • Intestinal Mucosa / metabolism
  • Intestinal Mucosa / microbiology*
  • Phylogeny
  • Sequence Analysis, DNA / methods*
  • Streptococcus suis / physiology*
  • Swine

Substances

  • Adhesins, Bacterial

Grants and funding

This study was supported by the EU-FP7 program ANTIGONE (Project No. FP7-278976). The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.