Poster Presentation 20th Lancefield International Symposium on Streptococci and Streptococcal Diseases 2017

The Streptococcus suis serotype 2 lipoproteins, but not the lipoteichoic acid, are important activators of the innate immune response (#149)

Jean-Philippe Auger 1 , Nicolas Gisch 2 , David Roy 1 , Marcelo Gottschalk 1
  1. University of Montreal, St-Hyacinthe, Quebec, Canada
  2. Research Center Borstel, Borstel, Germany

Streptococcus suis serotype 2 is an important porcine bacterial pathogen and zoonotic agent responsible for sudden death (pigs), septic shock (humans), and meningitis (both species). Alongside peptidoglycan, lipoteichoic acids (LTA) are a major constituent of the Gram-positive cell wall and have been previously suggested to contribute to the virulence of S. suis. Moreover, lipoproteins (LP), which are often co-purified with LTA, are considered to be major activators of the innate immune response. However, the immunostimulatory properties of the S. suis LTA, taking into account the potential presence of contaminating LPs, have not been investigated in detail. Herein, LTA preparations from S. suis were extensively purified and used to stimulate dendritic cells (DCs), which are sentinel innate immune cells implicated in the S. suis infection. Results demonstrated that LTA preparations induce important and dose-dependent levels of the pro-inflammatory mediators TNF, IL-6, CCL3, and CXCL1 from DCs. In order to evaluate the role of contaminating LPs, preparations were treated with H2O2, which oxidizes LPs to render them biologically inactive. Treatment resulted in a significant reduction of pro-inflammatory mediator production, indicating that contaminating co-purified LPs are the main source of DC activation. In accordance, DCs deficient for the Toll-like receptor 2 (TLR2), which is the main receptor involved in the recognition of bacterial LPs, produced significantly lower levels of cytokines. In conclusion, this study demonstrates that the S. suis surface LPs are important inducers of pro-inflammatory mediators by DCs through TLR2 activation, unlike the LTA.