Mégraud F
Laboratoire de Bactériologie-Enfants, Hôpital Pellegrin, Bordeaux, France.
Eur J Gastroenterol Hepatol. 1994 Dec;6 Suppl 1:S5-10.
To review the various toxic factors produced directly or indirectly by Helicobacter pylori and discuss their relative importance in H. pylori infection.
The toxic factors produced by H. pylori can act at different levels. At the epithelial cell level H. pylori enzymes generate toxic molecules: ammonia (urease), lysolecithin (phospholipases) and acetaldehyde (alcohol dehydrogenase). The harmful effects of ammonia have been studied the most intensively and seem to be a likely mechanism of pathogenicity. A vacuolating cytotoxin is expressed in 50-60% of the strains while the gene is present in all. Despite the fact that its potential toxic effect is low, the cytotoxin is associated with ulcer development. Another protein, CagA is a marker for the presence of the toxin. H. pylori can also produce a hemolysin, a platelet-activating factor and a factor that alters parietal cell function. At the mucus level, it does not seem that H. pylori enzymes degrade mucin, and the thinness of the layer could be due to inhibition of mucus exocytosis.
H. pylori have a wide range of toxic factors which can act together but no one factor is considered sufficient alone to explain the observed lesions.
回顾幽门螺杆菌直接或间接产生的各种毒性因子，并讨论它们在幽门螺杆菌感染中的相对重要性。
幽门螺杆菌产生的毒性因子可在不同水平发挥作用。在上皮细胞水平，幽门螺杆菌的酶可产生毒性分子：氨（尿素酶）、溶血卵磷脂（磷脂酶）和乙醛（乙醇脱氢酶）。对氨的有害作用研究最为深入，似乎是一种可能的致病机制。50% - 60%的菌株表达一种空泡毒素，而所有菌株都存在该基因。尽管其潜在毒性作用较低，但该毒素与溃疡的发生有关。另一种蛋白质CagA是毒素存在的标志物。幽门螺杆菌还可产生溶血素、血小板激活因子以及一种改变壁细胞功能的因子。在黏液水平，幽门螺杆菌的酶似乎不会降解黏蛋白，黏液层变薄可能是由于黏液胞吐作用受到抑制。
幽门螺杆菌有多种毒性因子，它们可共同发挥作用，但没有一种因子被认为单独就足以解释所观察到的病变。
