Research for comparison of VacA in H. pylori infectious diseases

持续感染幽门螺杆菌可引起慢性活动性胃炎，使黏膜易发生消化性溃疡，被认为参与胃癌和MALT淋巴瘤的发病机制。幽门螺杆菌分泌VacA，一种导致易感细胞空泡变性的细胞毒素。VacA中间的序列定义了两个家族，称为m1 VacA和m2 VacA，它们在细胞特异性上不同。由于s1/m2菌株产生低水平的毒素，很可能m1VacA。比m2VacA造成更多的上皮损伤。在本研究中，我们从菲律宾和日本的幽门螺杆菌引起的各种疾病患者分离的幽门螺杆菌培养基中纯化了m1vaca和m2VacA。与m1VacA类似，m2VacA被酸或碱激活，从而增强其与细胞的结合，这是易感细胞形成液泡的第一步。免疫沉淀实验显示，活化的m2VacA与miVacA类似，在az - 521细胞中结合两种受体样蛋白酪氨酸磷酸酶RPTPa和RPTP(3)，提示活化的m2VacA和m1VacA可能与幽门螺杆菌感染后的胃肠道疾病有关。我们的研究结果。我们发现m2VacA是重要的毒力因子，并支持Go等人报道的含有m2VacA的幽门螺杆菌菌株与十二指肠溃疡相关的发现[Go， m.f., Cissell， L., and Grayham， D. Y.(1998)]。[j].中国生物医学工程学报，1999,19(2):444 - 444。

Persistent infection with Helicobacter pylori causes chronic active gastritis, which predisposes the mucosa to peptic ulceration, and is believed to participate in the pathogenesis of gastric carcinoma and MALT lymphoma. H pylori secretes VacA, a cytotoxin that causes vacuolar degeneration of susceptible cells. Sequence in the middle of VacA defines two families, termed m 1 VacA and m2 VacA, which differ in cell specificity. Since s1/m2 strains produce low levels of toxin, it is likely that m1VacA. is responsible for more epithelial damage than m2VacA.In this study, we purified m 1 VacA and m2VacA from culture medium from H. pylori isolated from patients suffering from H. pylori-induced various diseases in Philippine and Japan.Similar to m1VacA, m2VacA is activated by acid or alkali, thereby enhancing its binding cells, the initial step in vacuole formation in susceptible cells. Immunoprecipitation experiments showed that activated m2VacA, similar to miVacA, binds to two receptor-like protein tyrosine phosphatases, RPTPa and RPTP(3 in AZ-52 1 cells, suggesting that activated m2VacA as well as m1VacA may contribute to gastrointestinal disease following H. pylori infection.Our results. lead that m2VacA is a significant virulence factor and support the finding that H. pylori strains with m2VacA is associated with duodenal ulcer reported by Go et al. [Go, M. F., Cissell, L., and Grayham, D. Y. (1998) Scand. J. Gastroenterol. 33, 132-136].