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直肠黏膜的器官培养:腹腔疾病中麸质的体外激发试验

Organ culture of rectal mucosa : in vitro challenge with gluten in celiac disease.

作者信息

Mazzarella G, Paparo F, Maglio M, Troncone R

机构信息

Istituto di Scienze dell'Alimentazione CNR, Avellino, Italy.

出版信息

Methods Mol Med. 2000;41:163-73. doi: 10.1385/1-59259-082-9:163.

Abstract

Celiac disease is sustained by an immunological process that mainly affects the jejunal mucosa (1). Nonetheless, jejunum is not the only site of the gastrointestinal tract that is involved in celiac disease. In recent years, Ensari and colleagues (2,3), by using immunohistochemical analysis and computerized image analysis for numerical quantitation, have significantly contributed to a definitive and clear demonstration of a celiac disease-associated "proctitis," and its gluten dependence. Morphometry has shown increased populations of plasma cells, lymphocytes, and mast cells in the rectal mucosa of untreated patients, with these changes being reverted, with the sole exception of mast cells, by dietary treatment (2). The immunohistochemical approach has demonstrated highly significant increases in CD3(+) and γδ(+) lymphocytes within both the lamina propria and the epithelium. Mononuclear cells, both lymphocytes (CD3(+)) and macrophages (CD68(+)) expressing interleukin-2 (IL-2) receptors (CD25(+)), have been found to be increased in the lamina propria, usually immediately below the basal lamina. Enterocytes have been noted to be positive for major histocompatibility complex class II display, a pattern usually absent in normal colon. Furthermore, increased expression of vascular cell adhesion molecule-1 (VCAM-1) molecules in the rectal mucosa of untreated, compared to either treated celiac rectum or control mucosae, has been reported (3). As a whole, these data suggest, analogously to jeunum, an ongoing T-cell-dependent, cell-mediated immune response in the rectal mucosa.

摘要

乳糜泻由一个主要影响空肠黏膜的免疫过程维持(1)。然而,空肠并非胃肠道中唯一参与乳糜泻的部位。近年来,恩萨里及其同事(2,3)通过使用免疫组织化学分析和计算机图像分析进行数值定量,为明确且清晰地证明与乳糜泻相关的“直肠炎”及其对麸质的依赖性做出了重大贡献。形态测量学显示,未经治疗的患者直肠黏膜中的浆细胞、淋巴细胞和肥大细胞数量增加,通过饮食治疗,除肥大细胞外,这些变化均可逆转(2)。免疫组织化学方法已证明固有层和上皮内的CD3(+)和γδ(+)淋巴细胞显著增加。在固有层中,通常在基底层下方紧邻处,已发现表达白细胞介素-2(IL-2)受体(CD25(+))的单核细胞,包括淋巴细胞(CD3(+))和巨噬细胞(CD68(+))数量增加。已注意到肠上皮细胞对主要组织相容性复合体II类分子呈阳性显示,这一模式在正常结肠中通常不存在。此外,据报道,与经治疗的乳糜泻直肠或对照黏膜相比,未经治疗的患者直肠黏膜中血管细胞黏附分子-1(VCAM-1)分子的表达增加(3)。总体而言,这些数据表明,与空肠类似,直肠黏膜中存在持续的T细胞依赖性细胞介导免疫反应。

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