Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Understanding Streptococcus suis serotype 2 infection in pigs through a transcriptional approach

ABSTRACT: Streptococcus suis serotype 2 is an important pathogen of pigs, and the disease it causes is characterized by meningitis, septicaemia and pneumonia with high mortality. The pathogen is also an emerging zoonotic agent and threatens humans that are exposed to pigs or their by-products. We investigated the response of PBMC (Peripheral Blood Mononuclear Cell), brain and lung tissues to infection with S. suis 2 strain SC19 by using the Affymetrix Porcine Genome Array. Six piglets free of S. suis 2 were allocated randomly to the infected group and the uninfected group. Each piglet of the infected group was intravenous injection with Streptococcus suis 2 strain SC19 at a dose of 3Ã105 colony-forming units (CFU). Each piglet of the noninfected group was treated similarly with an identical volume of PBS as control. At 24 h after challenge, the pigs were slaughtered and their brains, lungs and PBMC were collected with RNase-free equipment for microarray analysis.

ORGANISM(S): Sus scrofa

SUBMITTER: Xiao Shaobo

PROVIDER: E-GEOD-24889 | 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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Understanding Streptococcus suis serotype 2 infection in pigs through a transcriptional approach

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