Transcriptional immune response of PRRSV-infected porcine dendritic cells and monocytes to Streptococcus suis infection
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ABSTRACT:
ORGANISM(S): Sus scrofa
PROVIDER: GSE75687 | GEO | 2016/06/01
SECONDARY ACCESSION(S): PRJNA305053
REPOSITORIES: GEO
Similar Datasets
Project description:We investigated for the first time the in vitro response of PRRSV-infected porcine DCs and monocytes to S. suis. We first assessed the effect of PRRSV infection on the phagocytosis and intracellular survival of S. suis by these two cell populations. We then used a genomic approach to compare the gene expression profiles of both type of cells infected with S. suis, with or without a previous infection with PRRSV. Total RNA obtained from porcine monocytes and dendritic cells infected with S. suis, PRRSV, or S. suis & PRRSV. Four replicates in all groups.
2016-06-01 | E-GEOD-75687 | biostudies-arrayexpress
Project description:The goal of this study was to produce a deep, global analysis of gene expression changes that occured following infection of normal porcine alveolar macrophages (PAMs) with PRRSV. The goal was to examine the gene expression changes to help determine the mechanisms that result in reduced function and immunosuppression observed in PRRSV-infected pigs. Keywords: time course of infection
2008-09-01 | GSE10346 | GEO
Project description:The goal of this study was to produce a deep, global analysis of gene expression changes that occured following infection of normal porcine alveolar macrophages (PAMs) with PRRSV. The goal was to examine the gene expression changes to help determine the mechanisms that result in reduced function and immunosuppression observed in PRRSV-infected pigs. Keywords: time course of infection The PAMs were infected in culture at an MOI of 10 with PRRSV strains VR-2332 and incubated at 37C until 6, 12, 16 or 24 hours post infection. Total cellular RNA was collected from each at the appropriate time. SAGE libraries were prepared from each infected time point as well as from noninfected PAMs. The SAGE libraries were sequenced to at least 95,000 tags each.
2008-09-01 | E-GEOD-10346 | biostudies-arrayexpress
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.
2014-05-01 | GSE52172 | GEO
Project description:The current level of knowledge on transcriptome responses triggered by Caesalpinia sappan (CS) extract in porcine peripheral blood mononuclear cells (PBMCs) after porcine reproductive and respiratory syndrome virus (PRRSV) infection is limited. Therefore, in the present study, we aimed to detect significant genes and pathways involved in CS extract supplementation responsiveness of PBMCs after PRRSV infection. RNA sequencing was conducted on PBMCs, which were isolated from six weaned piglets. The resultant transcriptional responses were examined by mRNA sequencing. Differential expression analysis identified 263 and 274 differentially expressed genes (DEGs) between the PRRSV and CTRL groups, and the PRRSV+CS and CTRL groups, respectively. Among these, ZNF646 and KAT5 emerged as the most promising candidate genes, potentially influencing the interaction between PRRSV-infected PBMCs and CS extract supplementation through the regulation of gene networks and cellular homeostasis during stress. Two pathways were detected to be associated with CS extract supplementation responsiveness: the cellular response to stress pathway and the NF-kB signaling pathway. Consequently, our study reveals a novel mechanism underlying cellular stress response and the NF-κB signaling pathway in PRRSV-infected PBMCs, and identifies a potential application of CS extract for activating the NF-κB signaling pathway. In conclusion, by supplementing CS extract in PBMC cells infected with PRRSV, we found that CS extract modulates PRRSV infection by inducing cellular stress, which is regulated by the NF-κB signaling pathway. This induced stress creates an adverse environment for PRRSV survival. This study contributes to a deeper understanding of the therapeutic targets and pathogenesis of PRRSV infection. Importantly, our results demonstrate that CS extract has the potential to be a candidate for modulating PRRSV infection.
2024-11-18 | GSE277761 | GEO
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.
2014-05-01 | E-GEOD-52172 | biostudies-arrayexpress
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.
2014-03-18 | GSE40658 | GEO
Project description:Porcine reproductive and respiratory syndrome (PRRSV) is a devastating pathogen for the pig industry worldwide. PRRSV mainly infects porcine alveolar macrophage (PAM). In the present study, single-cell RNA sequencing (scRNA-seq) was employed to characterize the host transcriptome responses of PAMs infected with a virulent PRRSV strain in vivo and ex vivo. Increase ofpro-inflammatory and anti-apoptotic genes was correlated with the increase of infection (expression of the virus ORF7 transcript).
2023-11-01 | GSE216865 | GEO
Project description:We used microarrays to detail the global gene expression changes following apical infection of porcine choroid plexus epithelial cells (PCPEC) with Streptococcus suis (S. suis) We compared PCPEC either un-treated or infected with wild-type S. suis strain 10 or the acapsular strain 10cpsDEF, respectively, to determine global gene expression changes by microarray analysis
2011-08-14 | E-GEOD-23751 | biostudies-arrayexpress
Project description:The Porcine Reproductive and Respiratory Syndrome (PRRS) has an extensive impact on pig production. The causative virus (PRRSV) is divided in two species, PRRSV-1 (European origin) and PRRSV-2 (North American origin). Within PRRSV-1, PRRSV-1.3 strains such as Lena are more pathogenic than PRRSV-1.1 strains such as Flanders 13 (FL13). To date, the molecular interactions of PRRSV with primary lung mononuclear phagocytes (MNP) subtypes including conventional dendritic cells type 1 (cDC1) and type 2 (cDC2), monocyte-derived DCs (moDC) and parenchymal macrophages (PIM) have not been thoroughly investigated. Here, we analysed the transcriptome profiles of in vivo FL13-infected parenchymal MNP subpopulations and of in vitro FL13- and Lena-infected parenchymal MNP. The cell specific expression profiles of in vivo sorted cells correlated with their murine counterparts (AM, cDC1, cDC2, moDC) with the exception of PIM. Both in vivo and in vitro, FL13 infection altered the expression of a low number of host genes while in vitro infection with Lena confirmed the higher ability of this strain to modulate host response. Machine learning (ML) and GSEA analyses unraveled additional relevant genes and pathways modulated by FL13 infection that were not identified by conventional analyses. GSEA increased the cellular pathways enriched in FL13 dataset, but ML allowed a more complete comprehension of functional profiles during FL13 in vitro infection. Data indicated that cellular reprogramming differed upon Lena and FL13 infection, and that the latter keeps antiviral and inflammatory macrophages/DC functions silent, suggesting a different mechanism of pathogenesis during early infection.
2021-01-04 | GSE147632 | GEO