Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human polymorphonuclear neutrophils from patients with rheumatoid arthritis

ABSTRACT: Within a study RNA samples of SF PMN from 9 RA patients and of blood PMN from 4 healthy donors were analyzed for chemokine expression. The RNA samples were amplified and labelled red. Control samples (SigM5 cell culture) were labelled green. Each sample and control sample was co-hybrizated on a microarray with 780 inflammatory genes and 20 internal controls. The results identified a robust chemokine expression profile for SF PMN in RA. CCL3, CCL18, CXCL8 and CXCL10 were strongly overexpressed in SF PMN compared to blood PMN of healthy donors.

INSTRUMENT(S): Axon- GenePix4000B

ORGANISM(S): Homo sapiens

DISEASE(S): acute monoblastic leukaemia

SUBMITTER: Judith Auer

PROVIDER: E-MEXP-994 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Polymorphonuclear leukocytes (PMN) from patients with chronic granulomatous disease (CGD) fail to produce microbicidal concentrations of reactive oxygen species due to mutations in NOX2. Patients with CGD suffer from severe, life-threatening infections and inflammatory complications. Granulibacter bethesdensis is an emerging Gram-negative pathogen in CGD that resists killing by CGD PMN and inhibits PMN apoptosis through unknown mechanisms. Microarray analysis was used to study mRNA expression in normal and CGD PMN during incubation with G. bethesdensis and, simultaneously, in G. bethesdensis with normal and CGD PMN. We detected upregulation of anti-apoptotic genes (e.g., XIAP, GADD45B) and downregulation of pro-apoptotic genes (e.g., CASP8, APAF1) in infected PMN. Transcript and protein levels of inflammation and immunity-related genes were also altered. Upon interaction with PMN, G. bethesdensis altered expression of ROS-resistance genes in the presence of normal but not CGD PMN. Bacterial stress response genes, including ClpB, increased during phagocytosis by both normal and CGD PMN demonstrating responses to oxygen-independent PMN antimicrobial systems. Antisense knock down demonstrated that ClpB is dispensable for extracellular growth but is essential for bacterial resistance to both normal and CGD PMN. Metabolic adaptation of Granulibacter growth in PMN included upregulation of pyruvate dehydrogenase. Pharmacologic inhibition of pyruvate dehydrogenase by triphenylbismuthdichloride was lethal to Granulibacter. This study expands knowledge of microbial pathogenesis by Granulibacter in cells from permissive (CGD) and non-permissive (normal) hosts and identifies potentially druggable microbial factors, such as pyruvate dehydrogenase and ClpB, to help combat this antibiotic-resistant pathogen. pathogen time series 0-1-4-24 in CGD subjects and normals : host time series 0-1-4-24 in CGD subjects and normals non-infected and infected with Gb

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Transcription profiling of human polymorphonuclear neutrophils from patients with rheumatoid arthritis

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