Wadström T, Hirmo S, Borén T
Department of Medical Microbiology, University of Lund, Sweden.
Aliment Pharmacol Ther. 1996 Apr;10 Suppl 1:17-27. doi: 10.1046/j.1365-2036.1996.22164002.x.
Unlike Helicobacter felis and other Helicobacter species of animal origin, Helicobacter pylori colonizes the lower gastric mucin layer of the stomach and adheres to human gastric epithelial cells. It is still an open question if H. pylori can interact with specific glycoconjugates in the gastric mucin layer. It is possible that colonization of the oral cavity is a first step of a complex infectious process. Most likely resting or slow growing cells of H. pylori interact with Lewis blood group substances in the gastric mucin layer and on the epithelium. This initial colonization is probably followed by binding to specific cell surface glycoconjugates (glycoproteins and glycolipids such as GM3) and specific sialylated or highly sulphated molecules such as cell surface sulphatides and heparan sulphate. H. pylori may also bind to specific phospholipid molecules such as phosphatidylethanolamine on the gastric cells. The adhesion process of certain strains can stimulate 'close' cell adhesion including pedestal formation similar to the phenomenon typical for a special class of enterovirulent Escherichia coli called attaching effacing E. coli. After gastric cell destruction by ammonia and H. pylori toxins (such as the vacuolating toxin) H. pylori may colonize the extracellular matrix (ECM). This phenomenon seems to include binding of cell surface sialic acid specific haemagglutinin to one ECM component, i.e. laminin. It is also likely that H. pylori may use similar events to penetrate intercellular junctions of gastric epithelial cells. These adhesion-penetration phenomena also involve coating of the microbe with host proteins to escape the host immune system and initiate a chronic lifelong infection process.
与猫幽门螺杆菌及其他源自动物的幽门螺杆菌不同，幽门螺杆菌定殖于胃的胃黏液下层，并黏附于人类胃上皮细胞。幽门螺杆菌是否能与胃黏液层中的特定糖缀合物相互作用仍是一个悬而未决的问题。口腔定殖可能是复杂感染过程的第一步。很可能处于静止或生长缓慢状态的幽门螺杆菌细胞会与胃黏液层及上皮中的Lewis血型物质相互作用。这种初始定殖之后可能会接着与特定的细胞表面糖缀合物（糖蛋白和糖脂，如GM3）以及特定唾液酸化或高度硫酸化的分子（如细胞表面硫酸脑苷脂和硫酸乙酰肝素）结合。幽门螺杆菌还可能与胃细胞上的特定磷脂分子（如磷脂酰乙醇胺）结合。某些菌株的黏附过程可刺激“紧密”细胞黏附，包括形成基座，这类似于一类特殊的肠道致病性大肠杆菌（即黏附性侵袭性大肠杆菌）的典型现象。在胃细胞被氨和幽门螺杆菌毒素（如空泡毒素）破坏后，幽门螺杆菌可能定殖于细胞外基质（ECM）。这种现象似乎包括细胞表面唾液酸特异性血凝素与一种ECM成分（即层粘连蛋白）的结合。幽门螺杆菌也很可能利用类似事件穿透胃上皮细胞的细胞间连接。这些黏附 - 穿透现象还涉及用宿主蛋白包裹微生物，以逃避宿主免疫系统并引发慢性终身感染过程。
