Inflammatory bowel disease: the role of inflammatory cytokine gene polymorphisms
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- Joanna Balding
- Thrombosis and Haemostasis Laboratory, Institute of Molecular Medicine, Trinity Centre for Health Sciences, St James’s Hospital, Dublin 8, Ireland
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- Wendy J. Livingstone
- Thrombosis and Haemostasis Laboratory, Institute of Molecular Medicine, Trinity Centre for Health Sciences, St James’s Hospital, Dublin 8, Ireland
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- Judith Conroy
- Department of Genetics, Trinity College, Dublin 2, Ireland
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- Lesley Mynett-Johnson
- Department of Genetics, Trinity College, Dublin 2, Ireland
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- Donald G. Weir
- Department of Clinical Medicine, Trinity Centre for Health Sciences, St James’s Hospital, Dublin 8, Ireland
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- Nasir Mahmud
- Department of Clinical Medicine, Trinity Centre for Health Sciences, St James’s Hospital, Dublin 8, Ireland
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- Owen P. Smith
- Department of Haematology, Our Lady’s Hospital for Sick Children, Crumlin, Dublin 12, Ireland
Abstract
<jats:p>THE mechanisms responsible for development of inflammatory bowel disease (IBD) have not been fully elucidated, although the main cause of disease pathology is attributed to up-regulated inflammatory processes. The aim of this study was to investigate frequencies of polymorphisms in genes encoding pro-inflammatory and anti-inflammatory markers in IBD patients and controls. We determined genotypes of patients with IBD (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" alttext="$n = 172$" id="E1"><mml:mi>n</mml:mi><mml:mo>=</mml:mo><mml:mn>172</mml:mn></mml:math>) and healthy controls (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" alttext="$n = 389$" id="E2"><mml:mi>n</mml:mi><mml:mo>=</mml:mo><mml:mn>389</mml:mn></mml:math>) for polymorphisms in genes encoding various cytokines (interleukin (IL)-1β, IL-6, tumour necrosis factor (TNF), IL-10, IL-1 receptor antagonist). Association of these genotypes to disease incidence and pathophysiology was investigated. No strong association was found with occurrence of IBD. Variation was observed between the ulcerative colitis study group and the control population for the TNF-α-308 polymorphism (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" alttext="$p = 0.0135$" id="E3"><mml:mi>p</mml:mi><mml:mo>=</mml:mo><mml:mn>0.0135</mml:mn></mml:math>). There was also variation in the frequency of IL-6-174 and TNF-α-308 genotypes in the ulcerative colitis group compared with the Crohn's disease group (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" alttext="$p = 0.01$" id="E4"><mml:mi>p</mml:mi><mml:mo>=</mml:mo><mml:mn>0.01</mml:mn></mml:math>). We concluded that polymorphisms in inflammatory genes are associated with variations in IBD phenotype and disease susceptibility. Whether the polymorphisms are directly involved in regulating cytokine production, and consequently pathophysiology of IBD, or serve merely as markers in linkage disequilibrium with susceptibility genes remains unclear.</jats:p>
Journal
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- Mediators of Inflammation
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Mediators of Inflammation 13 (3), 181-187, 2004
Hindawi Limited
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Keywords
Details 詳細情報について
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- CRID
- 1363107368315959680
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- ISSN
- 14661861
- 09629351
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- Data Source
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- Crossref