Unknown,Transcriptomics,Genomics,Proteomics

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Carbohydrates Regulate Virulence Gene Expression in Streptococcus suis

ABSTRACT: 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.

ORGANISM(S): Streptococcus suis P1/7

SUBMITTER: Peter van Baarlen

PROVIDER: E-GEOD-40658 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Background: Swine influenza is a highly contagious viral infection in pigs affecting the respiratory tract that can have significant economic impacts. Streptococcus suis serotype 2 is one of the most important post-weaning bacterial pathogens in swine causing different infections, including pneumonia. Both pathogens are important contributors to the porcine respiratory disease complex. Outbreaks of swine influenza virus with a significant level of co-infections due to S. suis have lately been reported. In order to analyze a global response to the dual infection, we carried out a comprehensive gene expression profiling using a microarray approach to study the swine tracheal epithelial (NPTr) cell response to a co-infection with H1N1 swine influenza virus (swH1N1) and S. suis serotype 2. Results: Gene clustering showed that the swH1N1 and swH1N1/S. suis infections modified the expression of genes in a similar manner. Additionally, infection of NPTr cells by S. suis alone did not result in many differentially expressed genes compared to mock-infected cells. However, some important genes coding for inflammatory mediators, such as chemokines, interleukins, cell adhesion molecules and eicosanoids, were significantly upregulated in the presence of both pathogens comparing to infection with each pathogen taken individually. This synergy may also be the consequence of an increased adhesion/invasion of epithelial cells previously infected by swH1N1, as recently reported. Conclusion: In a co-infection situation, influenza virus would replicate in the respiratory epithelium inducing an inflammatory infiltrate comprised of mononuclear cells and neutrophils. Despite that these cells are unable to phagocyte and kill S. suis, they are highly activated by this pathogen. S. suis is not considered a primary pulmonary pathogen, but an exacerbated production of pro-inflammatory mediators during a co-infection with influenza virus may be of critical importance in the pathogenesis and outcome of this respiratory disease complex. Total RNA obtained from NPTr cells infected with S. suis, H1N1, or S. suis & H1N1. Four replicates in both groups.

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Carbohydrates Regulate Virulence Gene Expression in Streptococcus suis

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