hsdS , Belonging to the Type I Restriction-Modification System, Contributes to the Streptococcus suis Serotype 2 Survival Ability in Phagocytes
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 s...
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Published in | Frontiers in microbiology Vol. 8; p. 1524 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
Frontiers Media S.A
09.08.2017
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Subjects | |
Online Access | Get full text |
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Summary: | 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. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Edited by: Dongsheng Zhou, Beijing Institute of Microbiology and Epidemiology, China This article was submitted to Infectious Diseases, a section of the journal Frontiers in Microbiology Reviewed by: Francisco José Pallarés, Universidad de Murcia, Spain; Pontus Nordenfelt, Lund University, Sweden These authors have contributed equally to this work. |
ISSN: | 1664-302X 1664-302X |
DOI: | 10.3389/fmicb.2017.01524 |