B-218. OFS Mediates Protection of Streptococcus suis Against Phagocytosis by Polymorphonuclear Neutrophils

G. Ramachandran, P. Valentin-Weigand, C. G. Baums;
Tierärztliche Hochschule Hannover, Hannover, GERMANY.

OFS is a virulence factor of S. suis serotype 2 strains as recently demonstrated by us in experimental infections of piglets with a highly virulent wild-type and its isogenic ofs mutant strain. The objective of this study was to characterize the S. suis ofs mutant in its interaction with host cells in order to explain the attenuation of virulence. In preliminary experiments we showed that recombinant OFS selectively binds fibrinogen in plasma of different species. Therefore, we speculated that OFS might be involved in adhesion, invasion and/or resistance to phagocytosis. Different S. suis strains including a capsule-deficient ofs double mutant were used to address this question. Experiments with HEp-2 human epithelial cells failed to demonstrate a function of OFS in adhesion or invasion. However, overexpression of OFS on the surface of Lactococcus lactis mediated a moderate increase of adhesion. This is in agreement with our experiments suggesting OFS-mediated binding to immobilised but not soluable fibrinogen. Phagocytosis studies with porcine polymorphonuclear neutrophils (PMNs) and the different S. suis strains revealed a significant attenuation of the ofs mutant in protection against phagocytosis (mean survival factors: 1.69 for wt, 0.86 for the ofs and 0.61 for the capsular mutant). Interestingly, a moderately virulent serotype 9 wild type strain with two detected frameshift mutations in the ofs gene had a very low survival factor of 0.07 in this assay. In conclusion, this study suggests that OFS can mediate protection against phagocytosis of virulent serotype 2 strains. Future studies will have to reveal the mechanisms of protection and the relevance for strains of other serotypes.