Toll-Like Receptor 2-Independent Host Innate Immune Response against an Epidemic Strain of <i>Streptococcus suis</i> That Causes a Toxic Shock-Like Syndrome in Humans

<div><p><i>Streptococcus suis</i> is an emerging zoonotic agent causing meningitis and septicemia. Outbreaks in humans in China with atypical cases of streptococcal toxic shock-like syndrome have been described to be caused by a clonal epidemic <i>S. suis</i> strain characterized as sequence type (ST) 7 by multilocus sequence typing, different from the classical ST1 usually isolated in Europe. Previous <i>in vitro</i> studies showed that Toll-like receptor (TLR) 2 plays a major role in <i>S. suis</i> ST1 interactions with host cells. In the present study, the <i>in vivo</i> role of TLR2 in systemic infections caused by <i>S. suis</i> ST1 or ST7 strains using TLR2 deficient (TLR2^−/−) mice was evaluated. TLR2-mediated recognition significantly contributes to the acute disease caused by the highly virulent <i>S. suis</i> ST1 strain, since the TLR2^−/− mice remained unaffected when compared to wild type (WT) mice. The lack of mortality could not be associated with a lower bacterial burden; however, a significant decrease in the induction of pro-inflammatory mediators, as evaluated by microarray, real-time PCR and protein assays, was observed. On the other hand, TLR2^−/− mice infected with the epidemic ST7 strain presented no significant differences regarding survival and expression of pro-inflammatory mediators when compared to the WT mice. Together, these results show a TLR2-independent host innate immune response to <i>S. suis</i> that depends on the strain.</p>