Open AccessThe involvement of MsmK in pathogenesis of the Streptococcus suis serotype 2
Author(s) -
Tan MeiFang,
Liu WanQuan,
Zhang ChunYan,
Gao Ting,
Zheng LinLin,
Qiu DeXin,
Li Lu,
Zhou Rui
Publication year - 2017
Publication title -
microbiologyopen
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.881
H-Index - 36
ISSN - 2045-8827
DOI - 10.1002/mbo3.433
Subject(s) - virulence , pathogenesis , microbiology and biotechnology , biology , pathogen , mutant , streptococcus suis , serotype , virulence factor , phagocytosis , in vitro , strain (injury) , wild type , gene , immunology , genetics , anatomy
Streptococcus suis serotype 2 ( SS 2) is an important swine and human pathogen that causes global economic and public health problems. Virulent S. suis strains successfully maintain high bacterial concentrations in host blood and rapidly adapt to challenging environments within hosts. Successful survival in hosts is a major factor influencing the pathogenesis of SS 2. We have previously identified that SS 2 colonization in mouse brain is possibly affected by the ATP ase, MsmK of carbohydrate ATP ‐binding cassette ( ABC ) transporters because of carbohydrate utilization. In this study, the chain length of the msmK deletion mutant was longer than that of the wild type, and the former was significantly more susceptible than the latter when theses strains were exposed to mouse blood both in vivo and in vitro. The hemolytic activity of the mutant strain was decreased. Although the adhesion of the mutant to HE p‐2 cell lines was enhanced, the deletion of msmK impaired the abilities of SS 2 to resist phagocytosis and survive severe stress conditions. MsmK contributed to the survival and adaptation of SS 2 in host bloodstream. Therefore, MsmK was identified as a multifunctional component that not only contributed to carbohydrate utilization but also participated in SS 2 pathogenesis.