Eriksson Anders, Flach Carl-Fredrik, Lindgren Anders, Kvifors Eva, Lange Stefan
Department of Internal Medicine, Gastroenterology Unit, Sahlgren's University Hospital/Ostra, Göteborg, Sweden.
BMC Gastroenterol. 2008 Aug 12;8:34. doi: 10.1186/1471-230X-8-34.
The cause and pathophysiology of ulcerative colitis are both mainly unknown. We have previously used whole-genome microarray technique on biopsies obtained from patients with ulcerative colitis to identify 5 changed mucosal transcripts. The aim of this study was to compare mucosal expressions of these five transcripts in ulcerative colitis patients vs. controls, along with the transcript expression in relation to the clinical ulcerative colitis status.
Colonic mucosal specimens from rectum and caecum were taken at ambulatory colonoscopy from ulcerative colitis patients (n = 49) with defined inflammatory activity and disease extension, and from controls (n = 67) without inflammatory bowel disease. The five mucosal transcripts aldolase B, elafin, MST-1, simNIPhom and SLC6A14 were analyzed using quantitative real-time PCR.
Significant transcript differences in the rectal mucosa for all five transcripts were demonstrated in ulcerative colitis patients compared to controls. The grade of transcript expression was related to the clinical disease activity.
The five gene transcripts were changed in patients with ulcerative colitis, and were related to the disease activity. The known biological function of some of the transcripts may contribute to the inflammatory features and indicate a possible role of microbes in ulcerative colitis. The findings may also contribute to our pathophysiological understanding of ulcerative colitis.
溃疡性结肠炎的病因和病理生理学目前大多尚不明确。我们之前曾利用全基因组微阵列技术对溃疡性结肠炎患者的活检样本进行分析，确定了5种发生改变的黏膜转录本。本研究旨在比较溃疡性结肠炎患者与对照组中这5种转录本的黏膜表达情况，以及转录本表达与溃疡性结肠炎临床状态的关系。
在门诊结肠镜检查时，从患有明确炎症活动和疾病范围的溃疡性结肠炎患者（n = 49）以及无炎症性肠病的对照组（n = 67）中采集直肠和盲肠的结肠黏膜标本。使用定量实时PCR分析5种黏膜转录本醛缩酶B、弹性蛋白酶、MST-1、simNIPhom和SLC6A14。
与对照组相比，溃疡性结肠炎患者的直肠黏膜中所有5种转录本均存在显著差异。转录本表达水平与临床疾病活动相关。
溃疡性结肠炎患者的5种基因转录本发生改变，且与疾病活动相关。部分转录本已知的生物学功能可能导致炎症特征，并提示微生物在溃疡性结肠炎中可能发挥作用。这些发现也可能有助于我们对溃疡性结肠炎病理生理学的理解。
