How does inflammation cause Barrett's metaplasia?

被引:43
作者
Colleypriest, Benjamin J. [1 ]
Ward, Stephen G. [2 ]
Tosh, David [1 ]
机构
[1] Univ Bath, Ctr Regenerat Med, Dept Biol & Biochem, Bath BA2 7AY, Avon, England
[2] Univ Bath, Dept Pharm & Pharmacol, Bath BA2 7AY, Avon, England
基金
英国医学研究理事会;
关键词
NF-KAPPA-B; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; GASTROESOPHAGEAL-REFLUX; ESOPHAGEAL ADENOCARCINOMA; INTESTINAL METAPLASIA; EPITHELIAL-CELLS; HOMEOBOX GENE; SQUAMOUS EPITHELIUM; RISK-FACTOR; BILE-ACIDS;
D O I
10.1016/j.coph.2009.09.005
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Oesophageal adenocarcinoma conveys a poor prognosis and has a rapidly increasing incidence. Similarly, Barrett's metaplasia (a precursor lesion for oesophageal adenocarcinoma) has an increasing incidence. Both oesophageal adenocarcinoma and Barrett's metaplasia are more common in the context of inflammation as a result of acid and bile reflux. The cytokine profile of Barrett's metaplasia is predominantly a T-helper 2 response that contrasts with the T-helper 1 response in normal and inflamed oesophagus and normal intestine. A key transcription factor in the development of Barrett's metaplasia, CDX2, has recently been shown to be induced in response to inflammatory mediators. The mechanism for induction of CDX2 is dependent on nuclear factor kappa B, a crucial transcription factor in the inflammatory response. Understanding the role of oesophageal inflammation will provide important insight into the development of Barrett's metaplasia and oesophageal cancer.
引用
收藏
页码:721 / 726
页数:6
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