Karamanolis D G, Kyrlagkitsis Ioannis, Konstantinou K, Papatheodoridis G V, Karameris A, Mallas E, Ladas S D, Raptis S
Department of Gastroenterology, Tzanio Hospital, Pireas, Greece.
Hepatogastroenterology. 2007 Jun;54(76):1085-8.
BACKGROUND/AIMS: Ulcerative colitis (UC) constitutes a chronic inflammatory process of the colon of unknown etiology. Current data support a pivotal role of apoptosis in the evolution of pathogenesis of UC. We performed a prospective study in order to determine the role of Bcl-2, Bax and Bcl-x in the apoptotic pathway in UC.
We included 23 patients with UC and 11 controls. Histological severity of the disease was assessed according to the Sidney classification system. Patients in the UC group were divided in 2 groups according to histological severity of the disease. The TUNEL method was used for the in situ evaluation of apoptosis. Immunohistochemical staining was used for the detection of Bax, Bcl-2, Bcl-x. For the assessment of cellular proliferation we used the monoclonal antibody Ki67. Appropriate statistical methods were applied.
Overall 77 specimens were assessed; 57 from UC patients and 20 from controls. Bcl-2, Bax and Bcl-x were upregulated in the group of patients with UC compared to controls. Nevertheless, Bax in epithelial cells and Bcl-x in lymphocytes were downregulated in patients with moderate/severe disease (p = 0.029 and 0.04 respectively). A weak correlation between epithelial apoptosis and Bcl-x expression in lymphocytes (r = 0.31, p = 0.02) was found. An even weaker correlation was also noticed between the epithelial component apoptosis and Bax in lymphocytes (r = 0.02, p = 0.07).
Bcl-2/Bax system does not appear to be involved in the induction of apoptosis in UC. Activation of intraepithelial lymphocytes may be associated with epithelial apoptosis or simply represent epiphenomena related to the inflammatory process.
背景/目的:溃疡性结肠炎(UC)是一种病因不明的结肠慢性炎症性疾病。目前的数据支持细胞凋亡在UC发病机制演变中起关键作用。我们进行了一项前瞻性研究,以确定Bcl-2、Bax和Bcl-x在UC凋亡途径中的作用。
我们纳入了23例UC患者和11例对照。根据悉尼分类系统评估疾病的组织学严重程度。UC组患者根据疾病的组织学严重程度分为两组。采用TUNEL法进行凋亡的原位评估。免疫组织化学染色用于检测Bax、Bcl-2、Bcl-x。为评估细胞增殖,我们使用了单克隆抗体Ki67。应用了适当的统计方法。
共评估了77个标本;57个来自UC患者,20个来自对照。与对照相比,UC患者组中Bcl-2、Bax和Bcl-x上调。然而,中度/重度疾病患者上皮细胞中的Bax和淋巴细胞中的Bcl-x下调(分别为p = 0.029和0.04)。发现淋巴细胞中上皮细胞凋亡与Bcl-x表达之间存在弱相关性(r = 0.31,p = 0.02)。还注意到上皮成分凋亡与淋巴细胞中Bax之间的相关性更弱(r = 0.02,p = 0.07)。
Bcl-2/Bax系统似乎不参与UC中凋亡的诱导。上皮内淋巴细胞的激活可能与上皮细胞凋亡相关,或者仅仅代表与炎症过程相关的附带现象。