The Journal of infectious diseases · 2013
The contribution of suilysin to the pathogenesis of Streptococcus suis meningitis.
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Takeuchi Dan, Akeda Yukihiro, Nakayama Tatsuya, Kerdsin Anusak, Sano Yasuteru, Kanda Takashi, Hamada Shigeyuki, Dejsirilert Surang, Oishi Kazunori
Аннотация
BACKGROUND: Streptococcus suis is an emerging zoonotic pathogen, and causes sepsis and meningitis in humans. Although sequence type (ST) 1 and ST104 strains are capable of causing sepsis, ST1 strains commonly cause meningitis. In this study, we investigated the role of suilysin, a member of cholesterol-dependent cytolysins, in differential pathogenicity between ST1 and ST104 strains.
METHODS: The levels of transcription and translation of the sly gene and messenger RNA of both ST strains were compared by means of quantitative polymerase chain reaction and Western blotting. Survival rates and bacterial densities in brain were compared between mice infected with wild-type and sly-knockout ST1 strain. ST104 infections with or without complementation of suilysin were also assessed.
RESULTS: The amounts of suilysin produced by ST1 strains were much higher than those produced by ST104 strains. Lower production of suilysin by ST104 strains were attributed to the attenuated sly gene expression, which seemed to be associated with 2 nucleotide insertions in sly promoter region. Furthermore, suilysin contributed to the higher bacterial density and enhanced inflammation in brain and increased mortality.
CONCLUSIONS: Our data may explain why ST1 strains, but not ST104 strains, commonly cause meningitis and also suggest the contribution of suilysin to the pathogenesis of meningitis in humans.
METHODS: The levels of transcription and translation of the sly gene and messenger RNA of both ST strains were compared by means of quantitative polymerase chain reaction and Western blotting. Survival rates and bacterial densities in brain were compared between mice infected with wild-type and sly-knockout ST1 strain. ST104 infections with or without complementation of suilysin were also assessed.
RESULTS: The amounts of suilysin produced by ST1 strains were much higher than those produced by ST104 strains. Lower production of suilysin by ST104 strains were attributed to the attenuated sly gene expression, which seemed to be associated with 2 nucleotide insertions in sly promoter region. Furthermore, suilysin contributed to the higher bacterial density and enhanced inflammation in brain and increased mortality.
CONCLUSIONS: Our data may explain why ST1 strains, but not ST104 strains, commonly cause meningitis and also suggest the contribution of suilysin to the pathogenesis of meningitis in humans.