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.

Project description:Toxoplasma gondii is an obligate intracellular protozoan of severe threat to humans and livestock. Macrophages are the cell type preferentially infected by T. gondii in vivo. Protein phosphorylation is an important post-translational modification involved in diverse cellular functions. ARAF is member of the RAF family of serine/threonine protein kinases that is necessary for MAPK activation. Limited information is available about the level of protein phosphorylation variations and the roles of ARAF in macrophages with T. gondii infection, although our previous research found that ARAF knockout could reduce the apoptosis of porcine alveolar macrophages (3D4/21 cells) caused by T. gondii infection. Here, we used IMAC in combination with LC-MS/MS to profile the changes of phosphorylation in 3D4/21 cells and 3D4/21-ΔAraf cells upon Toxoplasma infection, respectively. A total of 1647 differentially expressed phosphorylated proteins (DEPPs) with 3876 differentially phosphorylated sites (DPSs) were identified in 3D4/21 cells with Toxoplasma infection (p3T group) when comparing 3D4/21 cells without parasite infection (pho3 group), and 959 DEPPs with1540 DPSs when comparing 3D4/21-ΔAraf cells with parasite infection (p3KT group). In addition, 552 DPSs corresponding to 406 DEPPs with the same phosphorylated sites were screened in the comparison p3T/pho3 vs. p3T/p3KT, which was identified as the DPSs and DEPPs related with ARAF. Remarkable functional properties of the DEPPs were discovered by GO analysis, KEGG pathway analysis, and STRING analysis. Of 406 DEPPs related with ARAF, 40 DEPPs corresponding to 57 DPSs involved in the apoptosis of 3D4/21 cells during Toxoplasma infection. Further analysis showed that the phosphorylation levels of MED1at serine1418, JUN at serine 73, MYC at serine 154, MCL1 at serine 65, and BAD at serine115 were upregulated in p3T, but downregulated in p3KT, suggesting that ARAF regulate phosphorylation of these sites to modulate the apoptosis of macrophages induced by Toxoplasma infection. These results revealed distinct responses of macrophages to Toxoplasma infection and the potential roles of ARAF in fighting against infection via phosphorylation of crucial proteins.

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.

Project description:A/Zhejiang/DTID-ZJU02/2009(H1N1) is a strain of the swine-origin influenza A(H1N1) virus isolated during the human swine flu outbreak of 2009. To analyze the miRNA expression profiles of A549 cells infected with A/Zhejiang/DTID-ZJU02/2009(H1N1) at 0, 24, 48, and 72 h post-infection (hpi) and investigate the relation between the miRNA expression profile and its pathogenesis, Human MicroRNA Array v2.0 was applied. At 24 hpi, 174 miRNAs were detected to change their expression compared with 0 hpi, 28 of them increased and 146 decreased. At 48 hpi, 214 changed miRNAs were detected, 21 of them increased and 193 decreased. At 72 hpi, 282 changed miRNAs were detected, 19 of them increased and 263 decreased. Targets of the 21 significantly differentially expressed miRNAs were analyzed by bioinformatics technology. The function categories of the predicted targets were analyzed by GO(Gene ontology) annotation. The signaling pathways involving the changed miRNAs were analyzed by KEGG(Kyoto Encyclopedia of Genes and Genomes) and GO annotation. Four key signaling pathways were identified, namely, the MAPK, apoptosis, JAK_STAT, and toll-like receptor signaling pathways. The apoptosis and MAPK signaling pathways were activated by all miRNAs, whereas the JAK_STAT and toll-like receptor signaling pathways were activated by some miRNAs but inhibited by the others, suggesting balance in the host–virus interaction. We also constructed and analyzed the protein-protein interaction network of all the predicted targets and found some key nodes. This finding provides a picture of miRNA expression in A549 cells infected with A/Zhejiang/DTID-ZJU02/2009(H1N1) as complete as possible, which may provide important information for investigation of H1N1 pathogenesis and therapeutic method. the miRNA expression profiles of A549 cells infected with A/Zhejiang/DTID-ZJU02/2009(H1N1) at 0, 24, 48, and 72 h post-infection (hpi) were analyzed and the relation between the miRNA expression profile and its pathogenesis was investigated.

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Porcine circovirus modulates swine influenza virus replication in pig trachea epithelial cells and porcine alveolar macrophages [NPTr]

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