Clyne M, Drumm B
Department of Paediatrics, University College Dublin, Our Ladys Hospital for Sick Children, Crumlin, Ireland.
FEMS Immunol Med Microbiol. 1996 Dec 1;16(2):141-55. doi: 10.1111/j.1574-695X.1996.tb00130.x.
Helicobacter pylori colonises the gastric mucosa of humans and causes both antral gastritis and duodenal ulcer disease. Exactly how H. pylori causes disease is not known but several pathogenic determinants have been proposed for the organism. These include adhesins, cytotoxins and a range of different enzymes including urease, catalase and superoxide dismutase. Surface molecules of H. pylori such as flagella, lipopolysaccharide, the urease enzyme and outer membrane proteins are putative adhesin molecules. While phosphatidylethanolamine and the Lewis(b) blood group antigen have been proposed as receptor molecules for the organism the exact mechanism by which H. pylori adheres to the gastric mucosa has still to be identified. Characterisation of the adhesins of H. pylori could lead to the development of adhesin analogues for use in the inhibition of colonisation and improved therapy for ulcer disease. In vivo studies with isogenic mutants which are incapable of adhering to the gastric mucosa would greatly clarify the significance of adherence. Such mutants could possibly be useful as a vaccine against infection with wild-type organisms.
幽门螺杆菌定殖于人类胃黏膜，可导致胃窦炎和十二指肠溃疡病。幽门螺杆菌究竟如何致病尚不清楚，但已提出该菌的几种致病决定因素。这些因素包括黏附素、细胞毒素以及一系列不同的酶，如尿素酶、过氧化氢酶和超氧化物歧化酶。幽门螺杆菌的表面分子，如鞭毛、脂多糖、尿素酶和外膜蛋白，都是假定的黏附素分子。虽然磷脂酰乙醇胺和Lewis(b)血型抗原已被提出作为该菌的受体分子，但幽门螺杆菌黏附于胃黏膜的确切机制仍有待确定。对幽门螺杆菌黏附素的特性进行研究，可能会开发出黏附素类似物，用于抑制定殖并改善溃疡病的治疗。使用不能黏附于胃黏膜的同基因突变体进行的体内研究，将极大地阐明黏附的重要性。此类突变体可能可用作预防野生型菌株感染的疫苗。
