hsdS , Belonging to the Type I Restriction-Modification System, Contributes to the Streptococcus suis Serotype 2 Survival Ability in Phagocytes

• Published in: Frontiers in microbiology Vol. 8; p. 1524
• Main Authors: Xu, Bin, Zhang, Ping, Li, Weiyi, Liu, Rui, Tang, Jinsheng, Fan, Hongjie
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Media S.A 09.08.2017
• Subjects: anti-phagocytosis; host specificity determinant specificity subunit; Microbiology; peptidoglycan-binding protein; reactive oxygen species; Streptococcus suis serotype 2; survival ability; survival ability; nitric oxide; peptidoglycan-binding protein; TNF-α; anti-phagocytosis; reactive oxygen species; host specificity determinant specificity subunit; Streptococcus suis serotype 2
• ISSN: 1664-302X; 1664-302X
• DOI: 10.3389/fmicb.2017.01524

serotype 2 (SS2) is an important zoonotic agent in swine and humans. Anti-phagocytosis and survival in phagocytic cells and whole blood is essential for bacteria to be pathogenic. In this study, the host specificity determinant specificity subunit (coded by ) of the Type I Restriction-Modification system and two peptidoglycan-binding proteins (coded by and ', respectively), which were simultaneously found to be subjected to transcript-level influence by , were identified to facilitate the anti-phagocytosis of SS2 to a microglia cell line BV2. Furthermore, they significantly enhanced its survival in BV2, whole blood, and a peroxidation environment (H O ) ( < 0.05), yet not in the acidic condition based on statistical analysis of the characteristic differences between gene mutants and wild-type SS2. In contrast, another specificity subunit, coded by ', that belonged to the same Type I Restriction-Modification system, only significantly reduced the survival ability of SS2 in the acidic condition when in the form of a gene-deleted mutant ( < 0.05), but it did not significantly influence the survival ability in other conditions mentioned above or have enhanced anti-phagocytosis action when compared with wild-type SS2. In addition, the mutation of significantly enhanced the secretion of nitric oxide and TNF-α by BV2 with SS2 incubation ( < 0.05). The SS2 was tested, and it failed to stimulate BV2 to produce IFN-γ. These results demonstrated that contributed to bacterial anti-phagocytosis and survival in adverse host environments through positively impacting the transcription of two peptidoglycan-binding protein genes, enhancing resistance to reactive oxygen species, and reducing the secretion of TNF-α and nitric oxide by phagocytes. These findings revealed new mechanisms of SS2 pathogenesis.