Piotrowski J, Skrodzka D, Slomiany A, Slomiany B L
Research Center, University of Medicine and Dentistry of New Jersey, Newark 07103-2400, USA.
Biochem Mol Biol Int. 1996 Oct;40(3):597-602. doi: 10.1080/15216549600201183.
H. pylori is recognized as a primary etiologic factor in the pathogenesis of gastric disease. Here, we assessed the effect of intragastric administration of H. pylori lipopolysaccharide at 50 and 200 micrograms dose on the epithelial cell apoptosis. Histological examination of the mucosal tissue two days following the treatment revealed that lipopolysaccharide at both doses induced in the rat stomach mucosal inflammatory responses typical of gastritis. The in situ DNA fragmentation assay demonstrated that these changes were associated with a marked increase in gastric epithelial cell apoptosis. The apoptotic index in the controls averaged 0.3%, and increased dramatically to 59% with the lipopolysaccharide at 50 micrograms dose, while at the 200 micrograms dose the apoptotic index of 71.9% was attained. The results point towards cell wall lipopolysaccharide as a virulence factor responsible for the induction of gastric epithelial cell apoptosis by H. pylori.
幽门螺杆菌被认为是胃部疾病发病机制中的主要病因。在此,我们评估了分别以50微克和200微克剂量胃内给予幽门螺杆菌脂多糖对上皮细胞凋亡的影响。治疗两天后对黏膜组织进行的组织学检查显示,两种剂量的脂多糖均在大鼠胃黏膜中诱发了典型的胃炎炎症反应。原位DNA片段化检测表明,这些变化与胃上皮细胞凋亡的显著增加有关。对照组的凋亡指数平均为0.3%,50微克剂量的脂多糖使其急剧增至59%,而200微克剂量时凋亡指数达到了71.9%。结果表明,细胞壁脂多糖是幽门螺杆菌诱导胃上皮细胞凋亡的一种毒力因子。