Piotrowski J, Morita M, Slomiany A, Slomiany B L
Research Center, New Jersey Dental School, University of Medicine and Dentistry of New Jersey, Newark 07103-2400.
Biochem Int. 1992 Jun;27(1):131-8.
The effect of lipopolysaccharide from H. pylori, a bacteria implicated in the etiology of gastric disease, on the gastric mucosal laminin-receptor interaction was investigated. The receptor protein, prepared from rat gastric epithelial cell membrane by affinity chromatography on laminin-coupled Sepharose, was radioiodinated, and incorporated into liposomes which exhibited specific affinity towards laminin-coated surface. The binding was inhibited by H. pylori lipopolysaccharide, which caused a maximum inhibition of 96% at 50 micrograms/ml. The inhibitory effect of the lipopolysaccharide was prevented by an antiulcer agent, ebrotidine that evoked essentially complete restoration in binding at 6-8 micrograms/ml. The results demonstrate that H. pylori through its lipopolysaccharide interferes with gastric epithelial cell-laminin binding, and that this disruptive effect could be successfully countered by ebrotidine.
对一种与胃病病因有关的细菌——幽门螺旋杆菌的脂多糖,对胃黏膜层粘连蛋白受体相互作用的影响进行了研究。通过在层粘连蛋白偶联琼脂糖上进行亲和层析从大鼠胃上皮细胞膜制备的受体蛋白,经放射性碘标记后,被包入对层粘连蛋白包被表面具有特异性亲和力的脂质体中。幽门螺旋杆菌脂多糖可抑制这种结合,在50微克/毫升时最大抑制率达96%。一种抗溃疡药物依罗替丁可防止脂多糖的抑制作用,在6 - 8微克/毫升时依罗替丁可使结合基本完全恢复。结果表明,幽门螺旋杆菌通过其脂多糖干扰胃上皮细胞与层粘连蛋白的结合,而依罗替丁可成功对抗这种破坏作用。