Project description:Streptococcus suis 2 Rgg-dependent transcription was analyzed. Microarray analysis was performed using RNA samples isolated from Streptococcus suis 2 wild-type strain 05ZYH33 as well as RNA isolated from 05ZYH33 rgg isogenic mutant strain during postexponential phases of growth.
Project description:Identification of Genes and Genomic Islands Correlated with High Pathogenicity through Tilling Microarray-Based Comparative Genomics in S. suis. Streptococcus suis is an important zoonotic pathogen that can cause meningitis and sepsis in both pigs and humans. S. suis isolates have been categorized into groups of different levels of pathogenicity, with sequence type (ST) ST1 clonal complex strains having a higher degree of virulence than other STs. However, the genetic basis of the differences in pathogenicity is still poorly understood. In this study, a comprehensive genomic comparison of 31 S. suis strains from different clinical sources with the genome sequence of the high pathogenicity (HP) strain GZ1 was conducted using NimbleGen’s tilling microarray platform.
Project description:Streptococcus suis is an important zoonotic pathogen that can cause meningitis and sepsis in both pigs and humans. In this study,we evaluated the genetic difference of 40 Streptococcus suis strains belonging to various sequence types by comparative genomic hybridization to identify genes associated with the variation in pathogenicity using NimbleGen’s tilling microarray platform. Application of Comparative Phylogenomics to Identify Genetic Differences Relating to Pathogenicity of Streptococcus suis
Project description:Two large-scale outbreaks of streptococcal toxic shock-like syndrome (STSLS) have revealed Streptococcus suis 2 (SS2) to be a severe, evolving pathogen in humans. We investigated the mechanism by which SS2 causes STSLS. The transcriptional regulator TstS up-regulated during experimental infection. Compared with the wild type 05ZY strain, the tstS deletion mutant (∆tstS) elicited reduced cytokine secretion in macrophages. In mice, tstS deletion decreased virulence, bacterial load, and cytokine production. Moreover, TstS expression in P1/7 strain led to induction of STSLS in the infected mice. This is noteworthy because although virulent, P1/7 does not normally induce STSLS. Through microarray-based comparative transcriptomics analysis, we found that TstS regulates multiple metabolism related genes and several virulence-related genes associated with immune evasion.
