Ehrmann Jirí, Kolek Antonín, Kod'ousek Rostislav, Zapletalová Jana, Lísová Sona, Murray Paul Gerard, Drábek Jirí, Kolár Zdenek
Laboratory of Molecular Pathology & Institute of Pathology, Palacký University, Hnevotínská 3 77515, Olomouc, Czech Republic.
Virchows Arch. 2003 May;442(5):453-61. doi: 10.1007/s00428-003-0794-2. Epub 2003 Apr 16.
Mechanisms leading to morphological changes of the small intestine during coeliac disease (CD) are not yet completely recognized; however, two main processes have been suggested recently: remodeling of mucosa by matrix metalloproteinases, and mucosal atrophy by apoptosis. The aim of this study was analysis of the expression of proteins regulating apoptosis in the small intestine of children with active CD (ACD) and potential CD (PCD). Jejunal biopsies of 43 children with PCD and untreated ACD and 21 control samples were analyzed by means of standard indirect immunohistochemical technique for Fas, Fas ligand (Fas-L), tissue transglutaminase (tTG), Bcl-2, and glutathione S-transferase (GST) expression. We found significantly lower numbers of Fas-expressing enterocytes in the ACD patients than in PCD patients and controls. Similarly, the number of Fas-positive mucosal lymphocytes was decreased in ACD when compared with PCD. The number of Fas-L- and tTG-expressing enterocytes and mucosal lymphocytes was higher in both PCD and ACD. On the other hand, the number of Bcl-2-positive mucosal lymphocytes in PCD as well as ACD was significantly lower. The expression of tTG in extracellular matrix was significantly higher in PCD and ACD when compared with controls. Our results showed that Fas and/or Fas-L, Bcl-2, and tTG may be involved in apoptotic pathways leading to mucosal atrophy in children with CD. tTG changes are in agreement with the presumed role of this protein in the pathogenesis of CD.
乳糜泻(CD)期间导致小肠形态变化的机制尚未完全明确;然而,最近提出了两个主要过程:基质金属蛋白酶介导的黏膜重塑和凋亡导致的黏膜萎缩。本研究的目的是分析调节活跃型CD(ACD)和潜在型CD(PCD)儿童小肠凋亡的蛋白质表达。采用标准间接免疫组织化学技术,对43例PCD和未经治疗的ACD儿童的空肠活检组织以及21份对照样本进行Fas、Fas配体(Fas-L)、组织转谷氨酰胺酶(tTG)、Bcl-2和谷胱甘肽S-转移酶(GST)表达分析。我们发现,ACD患者中表达Fas的肠上皮细胞数量显著低于PCD患者和对照组。同样,与PCD相比,ACD中Fas阳性黏膜淋巴细胞数量减少。PCD和ACD中表达Fas-L和tTG的肠上皮细胞及黏膜淋巴细胞数量均较高。另一方面,PCD和ACD中Bcl-2阳性黏膜淋巴细胞数量均显著降低。与对照组相比,PCD和ACD中细胞外基质中tTG的表达显著更高。我们的结果表明,Fas和/或Fas-L、Bcl-2和tTG可能参与了导致CD儿童黏膜萎缩的凋亡途径。tTG的变化与该蛋白在CD发病机制中的推测作用一致。