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: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.
Project description:Streptococcus suis is a major swine pathogen that can be transmitted to humans causing severe symptoms. A large human outbreak was described in China, where approximately 25% out of 215 infected humans developed an unusual streptococcal toxic shock-like syndrome (STSLS). Albeit increased expression of inflammatory mediators following infection by the Chinese S. suis strain was suggested as responsible for STSLS case severity, the mechanisms involved are still poorly understood. In this study, we investigated the host innate immune response to infection by either one of 3 strains of S. suis: 89-1591 (Canadian, intermediate virulence), P1/7 (European, high virulence), and SC84 (Chinese, epidemic strain). Using Illumina microarray and validating those results with qPCR and Luminex assay, infected mice showed elevated expression of mainly pro-inflammatory chemokine and cytokine genes. Generally, pro-inflammatory genes were expressed at a higher level in mice infected with S. suis strain SC84 > P1/7 > 89-1591. Interestingly, IFNγ was expressed at much higher levels only in mice infected with the S. suis strain SC84, which could potentially explain some of the STSLS symptoms. IFNγ-KO mice infected with SC84 showed better survival than WT mice while no differences was seen in mice infected with highly virulent P1/7 strain. Overall, our results show an important role of IFNγ in S. suis infections and might explain in part the increased virulence of SC84 responsible for a recent outbreak in China.
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 a major swine pathogen that can be transmitted to humans causing severe symptoms. A large human outbreak was described in China, where approximately 25% out of 215 infected humans developed an unusual streptococcal toxic shock-like syndrome (STSLS). Albeit increased expression of inflammatory mediators following infection by the Chinese S. suis strain was suggested as responsible for STSLS case severity, the mechanisms involved are still poorly understood. In this study, we investigated the host innate immune response to infection by either one of 3 strains of S. suis: 89-1591 (Canadian, intermediate virulence), P1/7 (European, high virulence), and SC84 (Chinese, epidemic strain). Using Illumina microarray and validating those results with qPCR and Luminex assay, infected mice showed elevated expression of mainly pro-inflammatory chemokine and cytokine genes. Generally, pro-inflammatory genes were expressed at a higher level in mice infected with S. suis strain SC84 > P1/7 > 89-1591. Interestingly, IFNγ was expressed at much higher levels only in mice infected with the S. suis strain SC84, which could potentially explain some of the STSLS symptoms. IFNγ-KO mice infected with SC84 showed better survival than WT mice while no differences was seen in mice infected with highly virulent P1/7 strain. Overall, our results show an important role of IFNγ in S. suis infections and might explain in part the increased virulence of SC84 responsible for a recent outbreak in China.
Project description:Streptococcus suis is a major swine pathogen that can be transmitted to humans causing severe symptoms. A large human outbreak was described in China, where approximately 25% out of 215 infected humans developed an unusual streptococcal toxic shock-like syndrome (STSLS). Albeit increased expression of inflammatory mediators following infection by the Chinese S. suis strain was suggested as responsible for STSLS case severity, the mechanisms involved are still poorly understood. In this study, we investigated the host innate immune response to infection by either one of 3 strains of S. suis: 89-1591 (Canadian, intermediate virulence), P1/7 (European, high virulence), and SC84 (Chinese, epidemic strain). Using Illumina microarray and validating those results with qPCR and Luminex assay, infected mice showed elevated expression of mainly pro-inflammatory chemokine and cytokine genes. Generally, pro-inflammatory genes were expressed at a higher level in mice infected with S. suis strain SC84 > P1/7 > 89-1591. Interestingly, IFNγ was expressed at much higher levels only in mice infected with the S. suis strain SC84, which could potentially explain some of the STSLS symptoms. IFNγ-KO mice infected with SC84 showed better survival than WT mice while no differences was seen in mice infected with highly virulent P1/7 strain. Overall, our results show an important role of IFNγ in S. suis infections and might explain in part the increased virulence of SC84 responsible for a recent outbreak in China.