GeneSet Information

Tier III GS75727 • CD - Comparison of the Cytokine, Chemokine, and Interferon Profiles of Chronic Human Inflammatory Disease

DESCRIPTION:

The genes that were significantly changed in expression in each disease are summarized in Table 1. Of interest is the upregu- lation of CCL11 (also known as eotaxin) exclusively in UC. While chemokines play a role in all inflammatory diseases, celiac disease is relatively independent of chemokine expres- sion. A unique feature for UC and CD is the increased transcript levels for the proinflammatory cytokine IL-1

LABEL:

CD - Cyto, Chemo, Interf

SCORE TYPE:

Effect

THRESHOLD:

0 <=> 10

GENES IN THRESHOLD:

26

DATE ADDED:

2010-06-30

DATE UPDATED:

2024-10-22

SPECIES:

AUTHORS:

van der Pouw Kraan TC, Zwiers A, Mulder CJ, Kraal G, Bouma G

TITLE:

Acute experimental colitis and human chronic inflammatory diseases share expression of inflammation-related genes with conserved Ets2 binding sites.

JOURNAL:

Inflammatory bowel diseases Feb 2009, Vol 15, pp. 224-35

ABSTRACT:

BACKGROUND: Ulcerative colitis (UC) and Crohn's disease (CD) are characterized by chronic inflammation of the gastrointestinal tract, with overlapping clinical characteristics and unknown etiology. We reasoned that in intestinal inflammation the initial activation of the innate immune response fails to resolve, finally resulting in uncontrolled chronic inflammatory bowel disease. METHODS: To identify the early inflammatory events in colitis that remain active in human chronic colitis, we analyzed the changes of the colonic transcriptome during acute experimental colitis and compared the outcome with previously published profiles of affected tissues from patients with UC and CD, and as a control for intestinal inflammation in general, tissues from celiac disease patients. Rheumatoid arthritis synovial tissues were included as a nonintestinal inflammatory disease. The expression profiles of each disease were analyzed separately, in which diseased tissues were compared to unaffected tissues from the same anatomical location. RESULTS: Gene ontology analysis of significantly regulated genes revealed a marked activation of immunity and defense processes in all diseases, except celiac disease, where immune activation is less prominent. The control region of upregulated genes contained an increase in Ets2 binding sites in experimental colitis, UC, and rheumatoid arthritis, and were associated with upregulated immune activity. In contrast, upregulated genes in celiac disease harbored the transcription factor binding site GLI, which binds to the Gli family of transcription factors involved in hedgehog signaling, affecting development and morphogenesis. CONCLUSION: Ets2 may be an important transcription factor driving inflammation in acute as well as chronic inflammatory disease PUBMED: 18942749
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Annotation Information

No sequence read archive data associated with this GeneSet.


Family (D005190)
Animals (D000818)
Humans (D006801)
Play and Playthings (D010988)
Immunity (D007109)
Mice (D051379)
Patients (D010361)
Gene Expression Profiling (D020869)
Celiac Disease (D002446)
Hedgehogs (D006364)
Role (D012380)
Binding Sites (D001665)
Proto-Oncogene Protein c-ets-2 (D050787)
Arthritis, Rheumatoid (D001172)
Tissues (D014024)
Inflammation (D007249)
Interleukin-1 (D007375)
Interferons (D007372)
Transcription Factors (D014157)
Methods (D008722)
Colitis, Ulcerative (D003093)
Colitis (D003092)
Inflammatory Bowel Diseases (D015212)
Gastrointestinal Tract (D041981)
Morphogenesis (D009024)
Immunity, Innate (D007113)
Crohn Disease (D003424)
Chemokines (D018925)
Arthritis (D001168)
bowel (MA:0001524)
chronic inflammation (MP:0002499)
colitis (MP:0002816)
intestinal inflammation (MP:0001858)
rheumatoid arthritis (MP:0003561)
arthritis (MP:0002993)
abnormal inflammatory response (MP:0001845)
transcription factor binding (GO:0008134)
innate immune response (GO:0045087)
immune response (GO:0006955)
binding (GO:0005488)
anatomical structure morphogenesis (GO:0009653)
signaling (GO:0023052)

Gene List • 26 Genes

Genes in threshold: 26

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Supported by NIH R01 AA18776 jointly funded by NIAAA and NIDA, and JAX Center for Precision Genetics NIH U54 OD 020351

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