Oral immunization with recombinant Helicobacter pylori urease induces secretory IgA antibodies and protects mice from challenge with Helicobacter felis.

Oral immunization with recombinant Helicobacter pylori urease induces secretory IgA antibodies and protects mice from challenge with Helicobacter felis.
复制标题

DOI:
10.1093/infdis/172.1.161
复制
发表时间:
1995-07
期刊:
The Journal of infectious diseases
影响因子:
--
通讯作者:
Cynthia K. Lee;R. Weltzin;W. Thomas;H. Kleanthous;T. Ermak;G. Soman;J. Hill;S. Ackerman;T. Monath
Cynthia K. Lee;R. Weltzin;W. Thomas;H. Kleanthous;T. Ermak;G. Soman;J. Hill;S. Ackerman;T. Monath
中科院分区:
其他
文献类型:
--
作者:
Cynthia K. Lee;R. Weltzin;W. Thomas;H. Kleanthous;T. Ermak;G. Soman;J. Hill;S. Ackerman;T. Monath

文献摘要

被引文献

相似文献

幽门螺杆菌是一种革兰氏阴性螺旋菌,是慢性浅表性(B型)胃炎和消化性溃疡的病因。对H. pylori作为无活性的重组蛋白在大肠杆菌中表达,纯化为直径约12 nm的550-600 kDa分子量的颗粒结构。口服5微克尿素酶和适当的粘膜佐剂,如大肠杆菌不稳定毒素。大肠杆菌感染的小鼠对猫螺杆菌攻击的保护率为60%~ 100%。保护作用与尿素酶分泌型伊加抗体水平相关。口服抗原与胃内给药一样有效或更好。胃肠外注射抗原或胃内给予高剂量抗原无佐剂引起血清IgG,但没有伊加抗体,并没有提供保护。重组尿素酶作为一种口服疫苗候选者值得进一步研究,作为一种预防人类幽门螺杆菌引起的慢性胃十二指肠疾病的方法。
Helicobacter pylori, a gram-negative spiral bacterium, is the cause of chronic superficial (type B) gastritis and peptic ulcer disease. The urease enzyme of H. pylori was expressed as an inactive recombinant protein in Escherichia coli, purified as particulate structures of 550-600 kDa molecular mass with a diameter of approximately 12 nm. Given orally, 5 micrograms of urease with an appropriate mucosal adjuvant, such as the labile toxin of E. coli, protected 60%-100% of mice against challenge with virulent Helicobacter felis. Protection correlated with the level of secretory IgA antibodies against urease. Oral administration of antigen was as effective or better than intragastric administration. Parenteral injection of antigen or intragastric administration of high-dose antigen without adjuvant elicited serum IgG but no IgA antibodies and did not confer protection. Recombinant urease as an oral vaccine candidate deserves further investigation as an approach to the prevention of Helicobacter-induced chronic gastroduodenal diseases in humans.