Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Gene expression profile of preclinical arthritis and its modulation by antigen-induced tolerance

ABSTRACT: During the course of adjuvant arthritis, maximal changes in gene expression were observed at the incubation phase. A major group of genes affected was related to immune activity. Tolerance induction by mycobacterial heat-shock protein 65 (Bhsp65), the disease-related antigen, caused upregulation of a large number of genes. These included immune activity genes as well as cell proliferation-related genes. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. The draining lymph node cells (LNC) were harvested from arthritic rats at different phases of adjuvant arthritis (incubation,peak and recovery). Also tested were LNC of naïve rats. LNC were tested ex vivo. Total RNA isolated from LNC was used for testing with affymetrix gene chip following manufacturer's instructions. Similarly, LNC of Bhsp65-tolerized rats harvested at incubation phase were tested with or without Bhsp65 restimulation in vitro. LNC of arthritic rats in incubation phase were similarly restimulated with Bhsp65 in vitro as controls, and the results compared with that of the tolerized rats.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Kamal Moudgil

PROVIDER: E-GEOD-31314 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

The gene expression profile of preclinical autoimmune arthritis and its modulation by a tolerogenic disease-protective antigenic challenge.

Yu Hua H Lu Changwan C Tan Ming T MT Moudgil Kamal D KD

Arthritis research & therapy 20110913 5

<h4>Introduction</h4>Autoimmune inflammation is a characteristic feature of rheumatoid arthritis (RA) and other autoimmune diseases. In the natural course of human autoimmune diseases, it is rather difficult to pinpoint the precise timing of the initial event that triggers the cascade of pathogenic events that later culminate into clinically overt disease. Therefore, it is a challenge to examine the early preclinical events in these disorders. Animal models are an invaluable resource in this reg ...[more]

PMID: 21914168

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Project description:Major toxicities of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) result from dysregulation of gene expression mediated by the aryl hydrocarbon receptor (AHR). Dioxin-like chemicals alter expression of numerous genes in liver but the specific genes whose dysregulation leads to toxicities such as wasting, hepatotoxicity and lethality have not been identified. We searched for genes that are most likely to be key to dioxin toxicity by using gene expression arrays to contrast hepatic gene expression after TCDD treatment in dioxin-sensitive rats (that carry wildtype AHR) with gene expression in H/W(Kuopio) rats which are highly resistant to dioxin toxicity due to a major deletion in the AHR's transactivation domain (TAD). The total number of TCDD-responsive genes was smaller in rats with the AHRH/W genotype than in rats with wildtype AHR. However, genes in the classic AH gene battery such as CYP1A1, CYP1A2 and CYP1B1 remained fully responsive to TCDD in AHRH/W rats; thus the TAD deletion selectively interferes with expression of a subset of hepatic genes rather than abolishing global AHR-mediated responses. Genes in the following functional categories differ in response to TCDD between dioxin-sensitive rats and dioxin-resistant rats: fatty acid oxidation, metabolism (xenobiotic, alcohol, amino acid, and fatty acid), phosphate transport, regulation of steroid biosynthesis, nitrogen compound catabolism, and generation of precursor metabolites and energy. Many of these differentially-responsive genes are integral parts of pathways such as: protein degradation and synthesis, fatty acid metabolism and synthesis, cytokinesis, cell growth, and apoptosis which may be part of mechanisms which lead to TCDD-induced wasting, hepatotoxicity, tumors, and death. These differentially-responsive genes are worthy candidates for further mechanistic studies to test their role in mediating or protecting from major dioxin toxicities. Experiment Overall Design: Four strains of rats were either treated with 100 ug/kg TCDD or cornoil vehicle and profiled at 19 hours, each with four replicates. Two strains were also analyzed at 3 hours, each with four replicates.

Dataset Information

Gene expression profile of preclinical arthritis and its modulation by antigen-induced tolerance

Publications

The gene expression profile of preclinical autoimmune arthritis and its modulation by a tolerogenic disease-protective antigenic challenge.

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