Wang Rong-Quan, Fang Dian-Chun
Department of Gastroenterology, Southwestern Hospital, Third Military Medical University, Chongqing, China.
J Gastroenterol Hepatol. 2006 Feb;21(2):425-31. doi: 10.1111/j.1440-1746.2005.04006.x.
Helicobacter pylori infection is one of the major causes of human gastric carcinoma and can disturb the gastric mucosa barrier. Mucins have not only lubricating and protecting functions, but are also related to signal transduction, turnover of gastric epithelium and carcinogenesis of gastric mucosa. The aim of this study was to investigate the relationship between H. pylori infection and aberrant mucin expression in patients with gastric carcinoma.
H. pylori infection was diagnosed by the Warthin-Starry staining method. Different kinds of mucins were detected using an immunohistochemical method.
Of 46 patients with gastric carcinoma, there were 26 patients who had H. pylori infection (56.5%). Of 21 pericancerous mucosas from the H. pylori-positive patients, 14 had MUC2 expression (66.7%), seven had strong MUC1 expression (+ + +) (33.7%), seven had strong MUC6 expression (+ + +) (33.3%), and five had strong MUC5AC expression (+ + +) (23.8%). In contrast, only six of 18 H. pylori-negative pericancerous mucosas had MUC2 expression (33.3%) (P < 0.05 compared with H. pylori-positive pericancerous mucosas), 12 had strong MUC1 expression (+ + +) in 16 H. pylori-negative pericancerous mucosas (75%) (P < 0.05), 11 had strong MUC6 expression (+ + +) in 16 H. pylori-negative pericancerous mucosas (68.8%) (P < 0.05), and 10 had strong MUC5AC expression (+ + +) in 14 H. pylori-negative pericancerous mucosas (71.4%) (P < 0.01). Of the H. pylori-positive cancerous tissues, 50% (13/26) had MUC1 expression and 38.5% (10/26) had MUC6 expression. In comparison, of the H. pylori-negative cancerous tissues, 80% (16/20) had MUC1 expression (P < 0.05) and 80% (16/20) had MUC6 expression (P < 0.01).
The results indicate that H. pylori infection can alter the expression of some mucin genes in pericancerous mucosa and cancerous tissues of gastric carcinoma, then destroy the gastric mucosa barrier.
幽门螺杆菌感染是人类胃癌的主要病因之一,可破坏胃黏膜屏障。黏蛋白不仅具有润滑和保护功能,还与信号转导、胃上皮更新及胃黏膜癌变有关。本研究旨在探讨胃癌患者幽门螺杆菌感染与黏蛋白异常表达之间的关系。
采用Warthin-Starry染色法诊断幽门螺杆菌感染。用免疫组织化学方法检测不同种类的黏蛋白。
46例胃癌患者中,26例有幽门螺杆菌感染(56.5%)。在21例幽门螺杆菌阳性患者的癌旁黏膜中,14例有MUC2表达(66.7%),7例有强MUC1表达(+++)(33.7%),7例有强MUC6表达(+++)(33.3%),5例有强MUC5AC表达(+++)(23.8%)。相比之下,18例幽门螺杆菌阴性癌旁黏膜中只有6例有MUC2表达(33.3%)(与幽门螺杆菌阳性癌旁黏膜相比,P<0.05),16例幽门螺杆菌阴性癌旁黏膜中有12例有强MUC1表达(+++)(75%)(P<0.05),16例幽门螺杆菌阴性癌旁黏膜中有11例有强MUC6表达(+++)(68.8%)(P<0.05),14例幽门螺杆菌阴性癌旁黏膜中有10例有强MUC5AC表达(+++)(71.4%)(P<0.01)。在幽门螺杆菌阳性癌组织中,50%(13/26)有MUC1表达,38.5%(10/26)有MUC6表达。相比之下,在幽门螺杆菌阴性癌组织中,80%(16/20)有MUC1表达(P<0.05),80%(16/2)有MUC6表达(P<0.01)。
结果表明,幽门螺杆菌感染可改变胃癌癌旁黏膜和癌组织中某些黏蛋白基因的表达,进而破坏胃黏膜屏障。