Vorobjova Tamara, Metsküla Kaja, Salumäe Liis, Uibo Oivi, Heilman Kaire, Uibo Raivo
Department of Immunology, Institute of Biomedicine and Translational Medicine, University of Tartu, Ravila 19, 51014, Tartu, Estonia.
Department of Pathology, Tartu University Hospital, Tartu, Estonia.
J Mol Histol. 2025 Jan 2;56(1):64. doi: 10.1007/s10735-024-10340-z.
Celiac disease (CD) is a chronic autoimmune disease of the small bowel mucosa that develops because of the altered immune response to gluten, which leads to intestinal epithelium damage and villous atrophy. However, studies on regeneration of the damaged small bowel mucosa and density of intestinal stem cells (ISC) in CD persons are still scarce. We aimed to evaluate the number of small bowel mucosa cells positive for LGR5, CD138/Syndecan-1, CD71 and CXCR3 in CD and in controls with normal bowel mucosa; to find relationship between these markers and degree of small intestinal atrophy and to compare these results with our previous data about the number of CD103 + , IDO + DCs, FOXP3 + Tregs, enterovirus (EV) density and serum zonulin level. The paraffin sections of the small bowel biopsies were obtained from 26 children with CD (median age 6.5 years), and from 20 controls with normal intestinal mucosa (median age 14.2 years) and from the tissue bank of the Department of Pathology of Tartu University Hospital (from 18 participants with CD including 14 children (median age 13.2 years) and from 11subjects with normal small bowel mucosa, including one child aged 4.8 years. The number of LGR5 + , CD71 + , CD138 + , and CXCR3 + cells was evaluated using immunohistochemistry. The median number of CD138 + and CXCR3 + cells was significantly higher in the small bowel mucosa in CD compared with normal mucosa (p = 0.0002 for CD138 and p = 0.006 for CXCR3). The median number of CD71 + cells was significantly higher in normal small bowel mucosa (p = 0.005). The number of LGR5 + cells did not differ between persons with CD and those with normal small bowel mucosa (p = 0.7). A markedly increased number of CD138 + and CXCR3 + cells in the small bowel mucosa of participants with CD confirms their role in the pathogenesis of this disease. There was no expected marked difference in the density of any of the studied markers between lower or higher grade of small bowel atrophy and level of tTG-IgA in CD.
乳糜泻（CD）是一种小肠黏膜的慢性自身免疫性疾病，其发病是由于对麸质的免疫反应改变，导致肠道上皮损伤和绒毛萎缩。然而，关于CD患者受损小肠黏膜再生及肠道干细胞（ISC）密度的研究仍然较少。我们旨在评估CD患者和小肠黏膜正常的对照者中，LGR5、CD138/多配体蛋白聚糖-1、CD71和CXCR3阳性的小肠黏膜细胞数量；找出这些标志物与小肠萎缩程度之间的关系，并将这些结果与我们之前关于CD103 +、吲哚胺2,3-双加氧酶（IDO）+树突状细胞（DC）、叉头框蛋白P3（FOXP3）+调节性T细胞（Tregs）、肠道病毒（EV）密度及血清连蛋白水平的数据进行比较。小肠活检组织的石蜡切片取自26例CD患儿（中位年龄6.5岁）、20例小肠黏膜正常的对照者（中位年龄14.2岁）以及塔尔图大学医院病理科的组织库（18例CD参与者，包括14名儿童（中位年龄13.2岁）；11例小肠黏膜正常的受试者，包括1名4.8岁儿童）。采用免疫组织化学方法评估LGR5 +、CD71 +、CD138 +和CXCR3 +细胞的数量。与正常黏膜相比，CD患者小肠黏膜中CD138 +和CXCR3 +细胞的中位数显著更高（CD138，p = 0.0002；CXCR3，p = 0.006）。正常小肠黏膜中CD71 +细胞的中位数显著更高（p = 0.005）。CD患者和小肠黏膜正常者之间LGR5 +细胞的数量没有差异（p = 0.7）。CD参与者小肠黏膜中CD138 +和CXCR3 +细胞数量显著增加，证实了它们在该疾病发病机制中的作用。在CD患者中，小肠萎缩程度较低或较高以及组织转谷氨酰胺酶IgA（tTG-IgA）水平不同时，所研究的任何标志物密度均未出现预期的显著差异。
