Macrophage Gene Expression Upon Infection with Anaplasma phagocytophilum in the Presence and Absence of the Tick Salivary Protein SL2
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE63647 | GEO | 2016/07/18
SECONDARY ACCESSION(S): PRJNA268526
REPOSITORIES: GEO
Similar Datasets
Project description:Previously, we observed that a tick salivary protein named sialostatin L2 (SL2) mitigates caspase 1-mediated inflammation upon Anaplasma phagocytophilum infection. Here we are performing next-generation sequencing to determine the global effect of SL2 upon A. phagocytophilum infection of macrophages. BMDMs were treated by 4 different conditions (including non-treated, treated by SL2, treated by Anaplasma, and by Anaplasma and SL2, each treatment was performed in triplicate) followed by the extraction of total RNA and deep sequencing by Illumina
2016-07-18 | E-GEOD-63647 | 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
Project description:Ticks are blood feeding arthropod ectoparasites that transmit pathogens, which cause diseases in humans and animals worldwide. In the past ten decades, the continuous human exploitation of environmental resources and the increase in human outdoor activities has promoted contact with arthropod vectors normally present in the wild, resulting in increased transmission of vector-borne pathogens. In addition, vector populations are expanding in response to climate change and human interventions that impact reservoir host movement and human exposure to infected vectors. Among these emerging vector-borne pathogens, Anaplasma phagocytophilum (Rickettsiales: Anaplasmataceae) has become an important tick-borne pathogen in the United States, Europe and Asia, with increasing numbers of infected people and animals every year. Diseases caused by A. phagocytophilum include human granulocytic anaplasmosis (HGA), equine and canine granulocytic anaplasmosis and tick-borne fever (TBF) in ruminants. The natural infection cycle of A. phagocytophilum is dependent upon the presence of infected vertebrate reservoir hosts and Ixodid tick vectors. In the United States and Europe the main vector species are Ixodes scapularis, Ixodes pacificus, and Ixodes ricinus, while a wide range of mammals, lizards, and birds serve as reservoir hosts for various A. phagocytophilum genotypes. A. phagocytophilum initially infects tick midgut cells and then subsequently develops in salivary glands for transmission to susceptible hosts during tick feeding where the pathogen infects granulocytic cells, primarily neutrophils. Anaplasma phagocytophilum develops within membrane-bound inclusions in the host cell cytoplasm. This pathogen has evolved with its tick and vertebrate hosts through dynamic processes involving genetic traits of the pathogen and hosts that collectively mediate pathogen infection, development, persistence, and survival. However, the mechanisms used by A. phagocytophilum for molecular mechanisms involved in tick-pathogen interactions have not been fully characterized. The objective of this study is to characterize the dynamics of the microRNA response in the tick vector Ixodes scapularis in response to A. phagocytophilum infection. To address this objective, the composition of tick microRNAs was characterize using RNA sequencing in I. scapularis tick cells in response to A. phagocytophilum infection. The discovery of these mechanisms provides evidence that a control strategy could be developed targeted at both vertebrate and tick hosts for more complete control of A. phagocytophilum and its associated diseases.
2016-03-19 | GSE79324 | GEO
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 cell’s 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
2016-01-06 | GSE68881 | GEO
Project description:We report differential gene expression with tissue-specific signatures in tick cell lines infected with Anaplasma phagocytophilum - transcriptional response to infection of I. scapularis ISE6 cells resembled that of tick hemocytes while the response in I. ricinus IRE/CTVM20 cells resembles that of tick midguts.
2017-01-01 | GSE76906 | GEO
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 cell’s 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.
2015-10-05 | PXD002181 | Pride
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 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: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: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