Infection by Helicobacter pylori expressing the BabA adhesin is influenced by the secretor phenotype
Infection by Helicobacter pylori expressing the BabA adhesin is influenced by the secretor phenotype
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DOI：
10.1002/path.2363
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发表时间：
2008-07-01
影响因子：
7.3
通讯作者：
David, L.
中科院分区：
文献类型：
--
作者：
Azevedo, M.;Eriksson, S.;David, L.
幽门螺杆菌（Hp）感染了世界上一半的人口，并导致各种胃病变，从胃炎到胃癌。我们的目的是评估分泌者和刘易斯状态在感染和体外粘附表达BabA粘附素的Hp中的意义。我们从葡萄牙北方招募了304名Hp感染者。收集胃活检、血液和唾液。采用聚合酶链反应（PCR）和免疫荧光法检测胃活检标本中BabA（+）Hp。进行了BabA表达Hp菌株对胃活检组织的体外粘附。通过Ulex（一种识别唾液和胃粘膜中分泌依赖性聚糖结构的凝集素）和刘易斯（a/B）抗体，以及通过鉴定FUT 2基因（G428 A）中的失活突变间接鉴定分泌状态。Hp感染的BabA状态与CagA和VacAs 1（P < 0.05）、Hp的细胞间定位（P < 0.01）以及活检中肠上皮化生（P < 0.05）和退行性改变（P < 0.005）的存在相关。BabA与胃活检的Ulex染色相关（P < 0.05），尽管不显著，但与FUT 2 G428 A失活多态性的纯合性缺失相关。FUT 2 G428 A突变的野生型或杂合子病例（p < 0.0001）、Ulex染色病例（p < 0.0001）和a（-）B（+）和a（-）B（-）分泌表型病例（p < 0.001）的体外Hp粘附性较高。总之，BabA+ Hp感染/粘附是分泌依赖性的，并与胃病变的严重程度相关。版权所有（C）2008大不列颠和爱尔兰病理学会。由John Wiley & Sons有限公司出版
Helicobacter pylori (Hp) infects half the world's population and causes diverse gastric lesions, from gastritis to gastric cancer. Our aim was to evaluate the significance of secretor and Lewis status in infection and in vitro adherence by Hp expressing BabA adhesin. We enrolled 304 Hp-infected individuals from Northern Portugal. Gastric biopsies, blood and saliva were collected. Polymerase chain reaction (PCR) and immunofluorescence were used to detect BabA(+) Hp in gastric biopsies. In vitro adherence by a BabA expressing Hp strain to gastric biopsies was performed. Secretor status was identified by Ulex, a lectin that recognizes secretor-dependent glycan structures in saliva and in gastric mucosa, and by Lewis(a/b) antibodies, and indirectly by identification of an inactivating mutation in the FUT2 gene (G428A). BabA status of infecting Hp was associated with CagA and VacAs1 (P < 0.05), intercellular localization of Hp (p < 0.01) and the presence of intestinal metaplasia (P < 0.05) and degenerative alterations (p < 0.005) in the biopsies. BabA was associated (P < 0.05) with Ulex staining of gastric biopsies and, although not significantly, to absence of homozygosity for FUT2 G428A inactivating polymorphism. In vitro Hp adherence was higher in cases wild-type or heterozygous for FUT2 G428A mutation (p < 0.0001), cases staining for Ulex (p < 0.0001) and a(-)b(+) and a(-)b(-) secretor phenotypes (p < 0.001). In conclusion, BabA+ Hp infection/adhesion is secretor-dependent and associated with the severity of gastric lesions. Copyright (C) 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.