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黏蛋白 Lewis 状态在儿童患者对幽门螺杆菌感染的耐药性中的作用。

Role of mucin Lewis status in resistance to Helicobacter pylori infection in pediatric patients.

机构信息

Mucosal Immunobiology and Vaccine Center, Sahlgrenska Academy, Gothenburg University, Box 435, 40530 Gothenburg, Sweden.

出版信息

Helicobacter. 2010 Aug;15(4):251-8. doi: 10.1111/j.1523-5378.2010.00765.x.

Abstract

BACKGROUND

Helicobacter pylori causes gastritis, peptic ulcer and is a risk factor for adenocarcinoma and lymphoma of the stomach. Gastric mucins, carrying highly diverse carbohydrate structures, present functional binding sites for H. pylori and may play a role in pathogenesis. However, little information is available regarding gastric mucin in children with and without stomach diseases.

MATERIALS AND METHODS

Expression of mucins and glycosylation was studied by immunohistochemistry on gastric biopsies from 51 children with and without H. pylori infection and/or peptic ulcer disease.

RESULTS

In all children, MUC5AC was present in the surface epithelium and MUC6 in the glands. No MUC6 in the surface epithelium or MUC2 was detected in any section. The Le(b) and Le(a) blood group antigens were present in the surface epithelium of 80% and 29% of children, respectively. H. pylori load was higher in Le(b) negative children than in Le(b) positive individuals (mean +/- SEM 17.8 +/- 3.5 vs 10.8 +/- 1.5; p < 0.05), but there was no correlation between Le(a) or Le(b) status and gastritis, nodularity, and gastric or duodenal ulcer (DU). Expression of sialyl-Le(x) was associated with H. pylori infection, and DU.

CONCLUSIONS

Mucin expression and glycosylation is similar in children and adults. However, in contrast to adults, pediatric H. pylori infection is not accompanied by aberrant expression of MUC6 or MUC2. Furthermore, the lower H. pylori density in Le(b) positive children indicates that H. pylori is suppressed in the presence of gastric mucins decorated with Le(b), the binding site of the H. pylori BabA adhesin.

摘要

背景

幽门螺杆菌可导致胃炎、消化性溃疡,也是胃腺癌和淋巴瘤的危险因素。胃粘蛋白携带有高度多样化的碳水化合物结构,可作为幽门螺杆菌的功能结合部位,可能在发病机制中发挥作用。然而,关于患有和不患有胃部疾病的儿童的胃粘蛋白的信息很少。

材料和方法

对 51 名儿童的胃活检组织进行免疫组织化学研究,这些儿童均有或无幽门螺杆菌感染和/或消化性溃疡病。

结果

在所有儿童中,MUC5AC 存在于表面上皮,MUC6 存在于腺体中。在任何切片中均未检测到表面上皮中的 MUC6 或 MUC2。Le(b)和 Le(a)血型抗原分别存在于 80%和 29%的儿童的表面上皮中。Le(b)阴性儿童的幽门螺杆菌负荷量高于 Le(b)阳性个体(平均值±SEM 17.8±3.5 比 10.8±1.5;p<0.05),但 Le(a)或 Le(b)状态与胃炎、结节、胃或十二指肠溃疡(DU)之间无相关性。唾液酸化-Le(x)的表达与幽门螺杆菌感染和 DU 相关。

结论

儿童和成人的粘蛋白表达和糖基化相似。然而,与成人不同的是,儿科幽门螺杆菌感染不伴有 MUC6 或 MUC2 的异常表达。此外,Le(b)阳性儿童中幽门螺杆菌密度较低表明,在胃粘蛋白上存在 Le(b)(幽门螺杆菌 BabA 粘附素的结合位点)时,幽门螺杆菌受到抑制。

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