Sus scrofa
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ABSTRACT:
PROVIDER: PRJNA116803 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Anaplasma phagocytophilum infects a wide variety of host species and causes the diseases granulocytic anaplasmosis in humans, horses and dogs and tick-borne fever in ruminants. The objective of this research was to characterize differential gene expression in wild boar naturally infected with A. phagocytophilum by microarray hybridization using the GeneChip® Porcine Genome Array Differential gene expression in wild boar naturally infected with A. phagocytophilum was chacarterized by microarray hybridization using the GeneChip® Porcine Genome Array and real-time RT-PCR.
2009-05-12 | E-GEOD-15766 | biostudies-arrayexpress
Project description:Anaplasma phagocytophilum infects a wide variety of host species and causes the diseases granulocytic anaplasmosis in humans, horses and dogs and tick-borne fever in ruminants. The objective of this research was to characterize differential gene expression in wild boar naturally infected with A. phagocytophilum by microarray hybridization using the GeneChip® Porcine Genome Array
2009-05-12 | GSE15766 | GEO
Project description:Preliminary characterization of gene expression in European wild boar naturally infected with Brucella suis
| PRJNA118697 | ENA
Project description:Anaplasma phagocytophilum is the causative agent of tick-borne fever (TBF) in ruminants and human, equine and canine granulocytic anaplasmosis. A. phagocytophilum modifies host gene expression and immune response. The objective of this work was to analyze differential gene expression in A. phagocytophilum-infected sheep using microarray hybridization and real-time RT-PCR in experimentally and naturally infected animals. Keywords: disease state analysis
2008-01-29 | GSE10286 | GEO
Project description:Brucella suis infects macrophages and dendritic cells. Wild boars act as reservoirs and carriers of Brucella suis biovar 2, and there is evidence that wild boar can be the main source of infection for domestic pigs through the venereal route. Transmission through this route could be an important path for disesease dissemination. The result from this study will contribute to the overall understanding of the molecular pathogenic mechanisms involved during Brucella suis infection in European wild boar. Experiment Overall Design: In this study we preliminarily characterized differential gene expression in European wild boar naturally infected with Brucella suis biovar 2 using Microarray hybridization and Real Time RT-PCR analysis. Since Brucella suis acts by infecting macrophages, we used spleen cells to analyze the gene expression response to Brucella suis infection.
2009-10-02 | E-GEOD-17492 | biostudies-arrayexpress
Project description:A whole genome tiling microarray based on the published sequence of the Anaplasma phagocytophilum (Ap) strain Hz genome was used to measure transcriptional activity of Ap grown to late stage in three cell lines representing the diversity of host cells naturally infected by Ap: two human cell lines, HL-60 (promyelocytic leukocyte) and HMEC-1 (microvascular endothelial), and the tick (Ixodes scapularis) cell line ISE6. Keywords: cell type comparison
2008-08-04 | GSE11487 | GEO
Project description:Anaplasma and Mycobacterium species are known to modify gene expression in ruminants. The objectives of this study were (a) to characterize global gene expression profiles in European red deer (Cervus elaphus) in response to Anaplasma ovis and A. ovis/Mycobacterium bovis/M. avium sub. paratuberculosis (MAP) infections, (b) to compare the expression of immune response genes between A. ovis- and A. ovis/M. bovis/MAP-infected deer, and (c) to characterize the differential expression of immune response genes identified in red deer in cattle infected with M. bovis and A. marginale. The results of this study showed that global gene differential expression in A. ovis- and A. ovis/M. bovis/MAP-infected deer results in the modification of common and pathogen-specific cellular biological processes. The differential expression of host immune response genes also showed pathogen-specific signatures and the effect of infection with multiple pathogens on red deer host immune response. These results suggested that intracellular bacteria from Anaplasma and Mycobacterium genera use similar mechanisms to infect and multiply within ruminant host cells while pathogen-specific mechanisms underline differences that could contribute to disease characterization and diagnosis in ruminants. A gene expression pre analysis was made in deers naturally infected with Anaplasma ovis and Mycobacterium complex using Affymetrix Bos taurus microarray to detect differentialy expressed genes. The immune response genes with variation in expression were analyzed by real time RT-PCR in the same samples and a bigger group of deers. A real time RT-PCR analysis was also made in Bos taurus naturally infected with Anaplasma marignale.
2010-12-31 | E-GEOD-21967 | biostudies-arrayexpress
Project description:Gene expression profiling of human promyelocytic cells in response to infection with Anaplasma phagocytophilum. Total RNA derived from 3DPI Anaplasma phagocytophilum-infected HL-60 cells was labeled with A647 and total RNA derived from 3DPI Mock-infected HL-60 cells was labeled with A546. For each, 5 µg of total RNA was labeled using Genisphere Array900, Alexa Fluor dyes and SuperscriptII. Slide scanned with ScanArray Express and images processed with GenePix Pro version 4.0. Normalized log ratios VALUES determined using R-project statistical environment (http://www.r-project.org) and Bioconductor (http://www.bioconductor.org) through the GenePix AutoProcessor (GPAP, http://darwin.biochem.okstate.edu/gpap) website (P. Ayoubi, unpublished results). Keywords: time-course
2005-02-25 | GSE1694 | GEO
Project description:Gene expression profiling of human promyelocytic cells in response to infection with Anaplasma phagocytophilum. Total RNA derived from 3DPI Anaplasma phagocytophilum-infected HL-60 cells was labeled with A647 and total RNA derived from 3DPI Mock-infected HL-60 cells was labeled with A546. For each, 5 µg of total RNA was labeled using Genisphere Array900, Alexa Fluor dyes and SuperscriptII. Slide scanned with ScanArray Express and images processed with GenePix Pro version 4.0. Normalized log ratios VALUES determined using R-project statistical environment (http://www.r-project.org) and Bioconductor (http://www.bioconductor.org) through the GenePix AutoProcessor (GPAP, http://darwin.biochem.okstate.edu/gpap) website (P. Ayoubi, unpublished results).
2010-06-10 | E-GEOD-1694 | biostudies-arrayexpress
Project description:Anaplasma phagocytophilum is an emerging zoonotic pathogen that causes human granulocytic anaplasmosis. These intracellular bacteria establish infection by affecting cell function in both the vertebrate host and the tick vector, Ixodes scapularis. Previous studies have characterized the tick transcriptome and proteome in response to A. phagocytophilum infection. However, in the post-genomic era, the integration of omics datasets through a systems biology approach allows network-based analyses to describe the complexity and functionality of biological systems such as host-pathogen interactions and the discovery of new targets for prevention and control of infectious diseases. This study reports for the first time a systems biology integration of metabolomics, transcriptomics and proteomics data to characterize essential metabolic pathways involved in the response of tick cells to A. phagocytophilum infection. The results showed that infection affected protein processing in endoplasmic reticulum and glucose metabolic pathways in tick cells. These results supported tick-Anaplasma co-evolution by providing new evidence of how tick cells limit pathogen infection, while the pathogen benefits from the tick cell response to establish infection. The results suggested that A. phagocytophilum induces protein misfolding to limit the tick cell response and facilitate infection, but requires protein degradation to prevent ER stress and cell apoptosis to survive in infected cells. Additionally, A. phagocytophilum may benefit from the tick cellâs ability to limit bacterial infection through PEPCK inhibition leading to decreased glucose metabolism, which also results in the inhibition of cell apoptosis that increases infection of tick cells. These results support the use of this experimental approach to systematically identify tick cell pathways and molecular mechanisms involved in tick-pathogen interactions Two samples with two replicates each were analyzed. Samples included Ixodes scapularis ISE6 cells uninfected (control) and infected with Anaplasma phagocytophilum human NY18 isolate.
2016-01-06 | E-GEOD-68881 | biostudies-arrayexpress