Department of Gastroenterology, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.
Eur J Gastroenterol Hepatol. 2009 Jul;21(7):781-6. doi: 10.1097/MEG.0b013e328309c76b.
Mannan-binding lectin (MBL) is an important constituent of the innate immune system, and deficiency of MBL has been reported to increase the overall susceptibility of an individual to infectious disease. Codon 54 G/A variant of exon 1 (B allele) affects MBL2 gene and alters its activity. We investigated the influence of MBL2 variant on the risk of gastroduodenal diseases and on the severity of Helicobacter pylori-induced gastritis in a Japanese population.
One hundred and two gastric ulcers, 48 duodenal ulcers, 275 nonulcer participants were included in this study. B allele of the MBL2 gene was detected by polymerase chain reaction based restriction fragment length polymorphism. The severity of the histological chronic gastritis in antral biopsy specimens were classified according to the updated Sydney system.
MBL2 B allele was significantly associated with severity of gastric mucosal atrophy and intestinal metaplasia (atrophy, G/G vs. G/A vs. A/A; P=0.02, A/A vs. others; P=0.009, intestinal metaplasia; G/G vs. G/A vs. A/A; P=0.03, A/A vs. others; P=0.004). When participants were divided into the following three groups according to the severity of gastric atrophy: the nonatrophic gastritis (NA) group, the severe atrophic gastritis (SA) group, and mild atrophic gastritis (MA) group, the frequency of A/A was significantly higher in the SA group than in others (SA vs. MA; odds ratio=8.42, 95% confidence interval=1.05-67.45, SA vs. others; odds ratio=10.06, 95% confidence interval=1.26-80.45).
Our data suggest that the MBL2 codon 54 B allele is associated with a risk of developing more severe gastric mucosal atrophy in H. pylori-infected Japanese patients.
甘露聚糖结合凝集素（MBL）是先天免疫系统的重要组成部分，已有报道称 MBL 缺乏会增加个体对感染性疾病的整体易感性。第 1 外显子的 54 号密码子 G/A 变体（B 等位基因）影响 MBL2 基因并改变其活性。我们在日本人群中研究了 MBL2 变体对胃十二指肠疾病风险和幽门螺杆菌引起的胃炎严重程度的影响。
本研究纳入了 102 例胃溃疡、48 例十二指肠溃疡和 275 例非溃疡参与者。通过聚合酶链反应基础的限制性片段长度多态性检测 MBL2 基因的 B 等位基因。根据更新的悉尼系统对胃窦活检标本的组织学慢性胃炎严重程度进行分类。
MBL2 B 等位基因与胃黏膜萎缩和肠化生的严重程度显著相关（萎缩，G/G 比 G/A 比 A/A；P=0.02，A/A 比其他；P=0.009，肠化生；G/G 比 G/A 比 A/A；P=0.03，A/A 比其他；P=0.004）。当根据胃萎缩的严重程度将参与者分为以下三组时：非萎缩性胃炎（NA）组、重度萎缩性胃炎（SA）组和轻度萎缩性胃炎（MA）组，SA 组 A/A 的频率明显高于其他组（SA 比 MA；比值比=8.42，95%置信区间=1.05-67.45，SA 比其他；比值比=10.06，95%置信区间=1.26-80.45）。
我们的数据表明，MBL2 密码子 54 B 等位基因与日本 H. pylori 感染患者发生更严重胃黏膜萎缩的风险相关。
