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Genome wide analysis of C57BL-6 mice infected with European strain (P1/7) of Streptococcus suis

ABSTRACT: 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, IFNM-NM-3 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. IFNM-NM-3-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 IFNM-NM-3 in S. suis infections and might explain in part the increased virulence of SC84 responsible for a recent outbreak in China. Total RNA obtained from spleen of C57BL/6 mice infected with Streptococcus suis strain P1/7 or mock-infected with THB. Four replicates in both groups.

ORGANISM(S): Mus musculus

SUBMITTER: Claude Lachance

PROVIDER: E-GEOD-41521 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome wide analysis of C57BL-6 mice infected with North-American strain (89-1591) of Streptococcus suis

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, IFNM-NM-3 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. IFNM-NM-3-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 IFNM-NM-3 in S. suis infections and might explain in part the increased virulence of SC84 responsible for a recent outbreak in China. Total RNA obtained from spleen of C57BL/6 mice infected with Streptococcus suis strain 89-1591 or mock-infected with THB. Four replicates in both groups.

2013-03-27 | E-GEOD-41520 | biostudies-arrayexpress

Genome wide analysis of C57BL-6 mice infected with Chinese strain (SC84) of Streptococcus suis

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, IFNM-NM-3 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. IFNM-NM-3-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 IFNM-NM-3 in S. suis infections and might explain in part the increased virulence of SC84 responsible for a recent outbreak in China. Total RNA obtained from spleen of C57BL/6 mice infected with Streptococcus suis strain SC84 or mock-infected with THB. Four replicates in both groups.

2013-03-27 | E-GEOD-41522 | biostudies-arrayexpress

Genome wide analysis of C57BL-6 mice infected with European strain (P1/7) of Streptococcus suis

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.

2013-03-27 | GSE41521 | GEO

Genome wide analysis of C57BL-6 mice infected with North-American strain (89-1591) of Streptococcus suis

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.

2013-03-27 | GSE41520 | GEO

Genome wide analysis of C57BL-6 mice infected with Chinese strain (SC84) of Streptococcus suis

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.

2013-03-27 | GSE41522 | GEO

Genome wide analysis of C57BL/6 mice and C57BL/6 TLR2-KO mice infected with European strain (P1/7) of Streptococcus suis

Project description:Streptococcus suis is an emerging zoonotic agent causing meningitis and septicemia. Outbreaks in humans in China with atypical cases of streptococcal toxic shock-like syndrome have been described to be caused by a clonal epidemic S. suis strain characterized as sequence type (ST) 7 by multilocus sequence typing, different from the classical ST1 usually isolated in Europe. Previous in vitro studies showed that Toll-like receptor (TLR) 2 plays a major role in S. suis ST1 interactions with host cells. In the present study, the in vivo role of TLR2 in systemic infections caused by S. suis ST1 or ST7 strains using TLR2 deficient (TLR2-/-) mice was evaluated. TLR2-mediated recognition significantly contributes to the acute disease caused by the highly virulent S. suis ST1 strain, since the TLR2-/- mice remained unaffected when compared to wild type (WT) mice. The lack of mortality could not be associated with a lower bacterial burden; however, a significant decrease in the induction of pro-inflammatory mediators, as evaluated by microarray, real-time PCR and protein assays, was observed. On the other hand, TLR2-/- mice infected with the epidemic ST7 strain presented no significant differences regarding survival and expression of pro-inflammatory mediators when compared to the WT mice. Together, these results show a TLR2-independent host innate immune response to S. suis that depends on the strain. Total RNA obtained from spleen of C57BL/6 mice or C57BL/6 TLR2-KO mice infected with Streptococcus suis strain P1/7. Four replicates in both groups.

2013-06-01 | E-GEOD-45861 | biostudies-arrayexpress

Streptococcus suis 05ZY: wt vs SSU05_0930 knockout strain

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.

2018-04-06 | GSE112779 | GEO

Genome wide analysis of C57BL-6 mice and C57BL/6 TLR2-KO mice infected with Chinese strain (SC84) of Streptococcus suis

2013-06-01 | E-GEOD-45862 | biostudies-arrayexpress

Gene expression analysis of human monocytic cells (THP-1) exposure to Streptococcus suis serotype 2

Project description:Streptococcus suis is an important zoonosis pathogen that causes significant economic losses worldwide characterized by meningitis, septicaemia, arthritis, bronchopneumonia endocarditis. Streptcoccus suis 2 strain SC19 was isolated in Sichuan province in China, during the outbreak in 2005. Septicemia is most popular symptoms for SC19 infection, and mortality is high. We used human acute monocytic leukemia cell line (THP-1) infected SC19 to analysis the pathomechanism of septicemia in SS2 infection.

2010-03-06 | GSE20508 | GEO

Carbohydrates Regulate Virulence Gene Expression in Streptococcus suis

Project description:Streptococcus suis is a major pig pathogen as well as an emerging zoonotic pathogen. Previous work has demonstrated that the S. suis extracellular amylopullulanase enzyme (ApuA) that degrades {alpha}-glucans also functions as an adhesin for porcine epithelial cells. To identify the mechanisms linking carbohydrate metabolism and virulence, we first compared the transcriptome of S. suis in minimal medium supplemented with glucose to minimal medium containing a complex carbohydrate pullulan as a carbon source. The relative expression of eighteen virulence genes including suilysin and apuA was increased during growth in presence of pullulan, compared to growth in glucose. Increased virulence potential of S. suis grown in pullulan was demonstrated using hemolytic assays and increased adhesion and invasion of porcine epithelial cells in vitro. A metabolic map of S. suis was generated and combined with transcriptome data to visualize the metabolic adaption of S. suis during adhesion and invasion of the porcine epithelial cells representing an in vitro model of infection. The role of carbon catabolite control in virulence gene regulation was investigated and the molecular mechanism of transcriptional regulation was elucidated for apuA. We demonstrate that relief of CcpA repression is a crucial transcriptional control mechanism linking carbohydrate mechanism and virulence. The model for the transcriptional regulation of two important virulence factors apuA and suilysin was verified by qPCR analysis of gene expression in S. suis recovered from the organs and blood of infected pigs. Four-condition experiment (bacteria grown in THB or in CM supplemented with three different carbon sources), at two different timepoints (early exponential or late exponential growth phase). One replicate per array.

2014-03-18 | E-GEOD-40658 | biostudies-arrayexpress

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