ArticleThe pharmacogenomics journal2002
Pharmacogenomic analysis of rhIL-11 treatment in the HLA-B27 rat model of inflammatory bowel disease.
Article in The pharmacogenomics journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 14 citations in OpenAlex.
- Colitis-induced IL11 promotes colon carcinogenesis.Carcinogenesis · 2021Article
- STAT3-Activating Cytokines: A Therapeutic Opportunity for Inflammatory Bowel Disease?Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2015Review
- Functional expression of the interleukin-11 receptor alpha-chain in normal colonic epithelium and colon cancer.International journal of colorectal disease · 2006Article
- A monoclonal antibody against kininogen reduces inflammation in the HLA-B27 transgenic rat.Arthritis research & therapy · 2005Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recombinant human interleukin-11 (rhIL-11) reduces the clinical signs and histological lesions of inflammatory bowel disease (IBD) in transgenic rats expressing the human major histocompatability complex (MHC) class I allele, HLA-B27. To elucidate the pharmacogenomic effects of rhIL-11 in this model, we examined the global gene expression pattern in inflamed colonic tissue before and following rhIL-11 treatment using oligonucleotide microarrays. In total, 175 disease-related genes were identified. Increased expression of genes involved in antigen presentation, cell death and inflammation, and decreased expression of metabolic genes was associated with disease. A total of 27 disease-related genes returned to normal expression levels following rhIL-11 treatment including the MHC class II gene RT1-DMbeta. rhIL-11 induced the expression of four intestinal epithelial growth factors. These gene expression patterns indicate that treatment of inflammatory bowel disease with rhIL-11 affects class II antigen processing and colonic epithelial cell proliferation and metabolism.
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