Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of human the treatments A. phagocytophilum-infected vs uninfected NB4 cells to determine the global impact of A. phagocytophilum infection in NB4 cells

ABSTRACT: THREE INDEPENDENT REPLICATES ARE THE CONTROL NON-INFECTED CELLS: GSM49939, GSM49940, GSM49941; THREE INFECTED INDEPEDENDENT REPLICATES: GSM49942, GSM49943, GSM49944

ORGANISM(S): Homo sapiens

DISEASE(S): reference

SUBMITTER: Joao Helbert Pedra

PROVIDER: E-GEOD-2600 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Modulation of NB4 promyelocytic leukemic cell machinery by Anaplasma phagocytophilum.

Pedra Joao H F JH Sukumaran Bindu B Carlyon Jason A JA Berliner Nancy N Fikrig Erol E

Genomics 20050901 3

Anaplasma phagocytophilum is a gram-negative obligate intracellular bacterium that persists within neutrophils. We assessed the impact of A. phagocytophilum infection in NB4 promyelocytic leukemic cells using high-density oligoarray, two-dimensional differential gel electrophoresis and liquid chromatography-mass spectrometry. Our Affymetrix data revealed that A. phagocytophilum altered the expression of transcription factors, cell adhesion molecules, signal transduction genes, and proinflammator ...[more]

PMID: 16005178

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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.

Dataset Information

Transcription profiling of human the treatments A. phagocytophilum-infected vs uninfected NB4 cells to determine the global impact of A. phagocytophilum infection in NB4 cells

Publications

Modulation of NB4 promyelocytic leukemic cell machinery by Anaplasma phagocytophilum.

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