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Intracranial Subarachnoidal Route of Infection for Investigating Roles of Streptococcus suis Biofilms in Meningitis in a Mouse Infection Model
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Critical role for Streptococcus suis cell wall modifications and suilysin in resistance to complement-dependent

Marie-Pier Lecours1, Marcelo Gottschalk, Mathieu Houde

  • 1Groupe de Recherche sur les Maladies Infectieuses du Porc and Centre de Recherche en Infectiologie Porcine, Faculté de Médecine Vétérinaire, Université de Montréal, St-Hyacinthe, Québec, Canada. mariela.segura@umontreal.ca

The Journal of Infectious Diseases
|August 19, 2011
PubMed

Insights

Streptococcus suis evades immune cells by altering its cell wall and releasing toxins. This pathogen

Area of Science:

  • Immunology
  • Microbiology
  • Bacteriology

Background:

  • Streptococcus suis is an emerging zoonotic pathogen causing septicemia and meningitis.
  • Limited knowledge exists on host immune responses to S. suis and its immune evasion strategies.

Purpose of the Study:

  • To investigate the modulation of dendritic cell (DC) functions by S. suis for the first time.
  • To identify specific virulence factors involved in S. suis immune evasion.

Main Methods:

  • Utilized S. suis knockout mutants lacking capsular polysaccharide (CPS).
  • Assessed mutants with impaired D-alanylation of lipoteichoic acid (LTA) and N-deacetylation of peptidoglycan (PG).
  • Evaluated bacterial resistance to complement-dependent killing by DCs and opsonophagocytosis.

Main Results:

  • CPS blocks DC phagocytosis and impairs cytokine release by hindering cell wall components.
  • LTA and PG modifications are crucial for resisting DC-mediated complement killing.
  • S. suis hemolysin contributes to reduced cytokine release and bacterial escape from phagocytosis.

Conclusions:

  • S. suis employs its virulence factors, including CPS, LTA, PG, and hemolysin, to modulate DC functions.
  • These factors enable S. suis to evade immune surveillance, contributing to its pathogenicity.

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