Abstract:[Background] Streptococcus suis type 2 (SS2) may cause meningitis, arthritis, and sepsis in humans and pigs, which not only brings great economic damage to the pig industry but also seriously threatens public health safety. In the previous study, using the phage display library technique, this team found that the protein encoded by Orf207 may be involved in SS2-induced meningitis; however, its specific role in the pathogenesis of SS2 is still unclear. [Objective] To explore the effect of the Orf207 gene on SS2 pathogenicity. [Methods] In this study, the homologous recombination system mediated by the thermosensitive suicide plasmid was used to construct the SC19 Orf207 gene deletion strain ΔOrf207 and its complementing strain CΔOrf207, after which the differences in biological characteristics such as growth characteristics, colony morphology, tissue colonization capacity, virulence, cell adhesion and invasion, and anti-macrophage phagocytosis between the deletion strain and the wild strain were systematically compared. [Results] Compared to wild strains, the deletion strain had shorter chain length and slower growth rate. Moreover, Orf207 deficiency significantly increased the survival rate of mice and reduced the colonization of bacteria in the blood, heart, liver, spleen, lung, kidney and brain, alleviating pathological damage to lung tissues. It also remarkably reduced the adhesion and invasion ability of SS2 to Hale cells and its anti-macrophage phagocytosis. [Conclusion] The above results indicate that gene Orf207 can significantly reduce the pathogenicity of SS2 to the host. The findings of this study enrich the pathogenesis of SS2 and provide a new target for the development of SS2 vaccine.
