Markesich D C, Anand B S, Lew G M, Graham D Y
Department of Medicine, Veterans' Affairs Medical Center, Houston, Texas, USA.
Gut. 1995 Mar;36(3):327-9. doi: 10.1136/gut.36.3.327.
The mechanism by which Helicobacter pylori undermines host defence mechanisms is unclear. Several in vitro studies using soluble mucins have suggested that H pylori may compromise mucus function. Gastric mucus gel was obtained from 13 H pylori infected patients; six untreated subjects and seven after eradication of the infection. Gastric mucus is a non-Newtonian substance in that its viscosity changes with changing rates of shear, requiring mucus viscosity to be measured in a rotational cone-plate microviscometer. Viscosity was measured at shear rates varying from 1.15 s-1 to 46 s-1. The gastric mucus viscosity was significantly higher in patients infected with H pylori compared with mucus gel obtained after eradication of the infection. The results of our study suggest that the previous studies using in vitro methods involving soluble mucins or its components may have lead to erroneous conclusions about the in vivo interactions of H pylori and gastric mucus gel. The present findings argue against the hypothesis that degradation of gastric mucus by H pylori is important in the pathogenesis of peptic ulcer.
幽门螺杆菌破坏宿主防御机制的机制尚不清楚。几项使用可溶性粘蛋白的体外研究表明，幽门螺杆菌可能会损害黏液功能。从13名幽门螺杆菌感染患者中获取胃黏液凝胶；6名未治疗的受试者和7名感染根除后的患者。胃黏液是一种非牛顿物质，其粘度会随着剪切速率的变化而改变，因此需要在旋转锥板微粘度计中测量黏液粘度。在1.15 s-1至46 s-1的剪切速率下测量粘度。与感染根除后获得的黏液凝胶相比，幽门螺杆菌感染患者的胃黏液粘度显著更高。我们的研究结果表明，先前使用涉及可溶性粘蛋白或其成分的体外方法的研究可能导致了关于幽门螺杆菌与胃黏液凝胶体内相互作用的错误结论。目前的研究结果与幽门螺杆菌降解胃黏液在消化性溃疡发病机制中起重要作用的假设相悖。
