Hopkins R J, Morris J G, Papadimitriou J C, Drachenberg C, Smoot D T, James S P, Panigrahi P
Division of Infectious Disease, University of Maryland School of Medicine, Baltimore 21201, USA.
Pathobiology. 1996;64(5):247-54. doi: 10.1159/000164055.
Adherence of Helicobacter pylori to gastric epithelial cells is thought to be important in the pathogenesis of infection and may be essential to maintain lifelong colonization. However, the factors responsible for adherence to gastric epithelial cells in vivo have not been characterized, and the significance of adherence to standard epithelial cell lines is unclear. Hemagglutination is also thought to be important in H. pylori adherence. However, no studies have clearly linked H. pylori hemagglutination or adherence to cultured epithelial cells to primary gastric epithelial cell adherence. Furthermore, it is not clear whether laboratory strains which have undergone multiple passages lose potential colonization factors. In this study, we examined the effect of serial laboratory passage on hemagglutination and correlated the hemagglutination characteristics of H. pylori strains to primary gastric cell adherence. Variable expression of hemagglutination was seen with serial laboratory passage of 15 strains. After 100 serial laboratory passages, all strains had lost hemagglutination activity. Hemagglutination was seen in association with adherence to primary gastric cells in vitro isolated from 2 patients. An association with ultrastructural intimate adherence was seen with HEp-2 cells, but not with gastric adenocarcinoma cells. Ultrastructural adherence was seen in corresponding antral biopsies of patients whose strains were hemagglutination positive, but hemagglutination was not associated with gastric inflammation. These data indicate that H. pylori hemagglutination is lost with serial passage and that hemagglutination may play a role in the attachment of H. pylori to gastric epithelial cells, but the role of adherence to chronic gastric inflammation is unclear.
幽门螺杆菌对胃上皮细胞的黏附被认为在感染发病机制中很重要,并且可能对维持终身定植至关重要。然而,体内负责黏附胃上皮细胞的因素尚未明确,对标准上皮细胞系黏附的意义也不清楚。血凝作用也被认为在幽门螺杆菌黏附中很重要。然而,尚无研究明确将幽门螺杆菌血凝或对培养上皮细胞的黏附与对原代胃上皮细胞的黏附联系起来。此外,尚不清楚经过多次传代的实验室菌株是否会失去潜在的定植因子。在本研究中,我们检测了连续实验室传代对血凝的影响,并将幽门螺杆菌菌株的血凝特性与对原代胃细胞的黏附相关联。15株菌株连续实验室传代后出现了血凝的可变表达。连续100次实验室传代后,所有菌株均失去了血凝活性。在从2名患者体外分离的原代胃细胞黏附中观察到了血凝现象。在HEp-2细胞中观察到与超微结构紧密黏附有关,但在胃腺癌细胞中未观察到。在菌株血凝呈阳性的患者相应胃窦活检中观察到超微结构黏附,但血凝与胃炎无关。这些数据表明,幽门螺杆菌血凝随着连续传代而丧失,血凝可能在幽门螺杆菌对胃上皮细胞的附着中起作用,但对慢性胃炎黏附的作用尚不清楚。