上海地区部分儿童幽门螺杆菌cagA、vacA、iceA基因型别分析

目的：了解上海部分地区儿童感染幽门螺杆菌（Hp）的cagA、vacA、iceA的基因亚型，探讨其与儿童上消化道疾病的关系。方法：收集2007年5月至2008年1月在我院行胃镜检查确诊Hp感染59例患者的胃黏膜组织，分别进行聚合酶链反应（PCR）检测cagA、vacA和iceA基因；病理检查胃窦黏膜炎症程度；酶联免疫吸附试验（ELISA）检测胃窦黏膜IFN-γ 和IL-4的含量。结果：cagA基因单独检出率为65%（37/57），vacAs1/m1单独检出率为19%（11/57）,vacAs1/m2单独检出率为40%（23/57），iceA1单独检出率为63%（36/57），iceA2单独检出率为19%（11/57），9%（5/57）的菌株iceA1 和iceA2均阳性。不同基因型菌株在慢性胃炎和消化性溃疡中的检出率差异无统计学意义（P>0.05）。不同基因型菌株与胃窦黏膜炎症的严重程度无关（P>0.05）。不同基因型菌株感染的胃窦黏膜IFN-γ、IL-4的含量差异亦无统计学意义（P>0.05）。结论：cagA/vacAs1/m2/iceA1为上海部分地区儿童中Hp的优势基因型。除了菌株因素外，宿主基因多态性、环境因素对于疾病的发生、发展也发挥了重要作用。［中国当代儿科杂志，2010，12（4）：267-271］

cagA, vacA and iceA genotypes of Helicobacter pylori isolated from children in Shanghai

Objective To investigate cagA,vacA and iceA genotypes of Helicobacter pylori(H.pylori)isolated from children suffering from gastric and duodenal diseases in Shanghai and to explore a possible genotype-phenotype correlation.Methods From May 2007 to January 2008,59 children were confirmed with Hp infection by gastroscopy.Biopsied specimens were taken from the gastric antrum.cagA,vacA and iceA genes were determined by PCR.The histological changes in the gastric mucosa were evaluated.The levels of IFN-γ and IL-4 in the gastric mucosa were measured using ELISA.Results cagA,vacAs1/m1,vacAs1/m2,iceA1 and iceA2 were found in 65%,19%,40%,63% and 19% of H.pylori strains,respectively.Both iceA1 and iceA2 were detected in 9% of strains.There were no statistical differences in the distribution of various genotypes between the children with chronic gastritis and peptic ulcer.No association was observed between the genotypes and the degree of inflammation of gastric mucosa.There were no significant differences in levels of IFN-γ and IL-4 in the gastric mucosa infected by different genotypes of H.pylori strains.Conclusions cagA/vacAs1/m2/iceA1 may be the commonest genotype combination of H.pylori in children from Shanghai.That there was no association between H.pylori genotypes and clinical variables suggests the potential role of host and environment factors in the development of clinical diseases at a later life.