Saldinger P F, Porta N, Launois P, Louis J A, Waanders G A, Bouzouréne H, Michetti P, Blum A L, Corthésy-Theulaz I E
Division of Gastroenterology, Department of Medicine, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
Gastroenterology. 1998 Oct;115(4):891-7. doi: 10.1016/s0016-5085(98)70261-6.
BACKGROUND & AIMS: Infection with Helicobacter induces a T helper type 1 response in mice and humans. Mice can be cured or protected from infection with Helicobacter by mucosal immunization with recombinant H. pylori urease B subunit (rUreB). This study characterizes the immune response of infected mice immunized with rUreB.
BALB/c mice were infected with H. felis. Two weeks later, they were orally immunized four times with rUreB and cholera toxin (CT) at weekly intervals. Controls were only infected or sham-immunized with CT. Animals were killed at various times after immunization. Splenic CD4(+) cells were obtained and cultured in vitro with rUreB to evaluate antigen-specific proliferation and induction of interferon gamma and interleukin 4 secretion.
All rUreB-immunized mice (n = 8) were cured from infection 3 weeks after the fourth immunization. Immunization induced a proliferative response of splenic CD4(+) cells, a progressive decrease in interferon gamma secretion, and a concomitant increase in interleukin 4 secretion after each immunization. A simultaneous increase in rUreB specific serum immunoglobulin G1 levels was observed in infected/immunized mice.
In BALB/c mice, therapeutic mucosal immunization with rUreB induces progressively a Th2 CD4(+) T cell response resulting in the elimination of the pathogen.
幽门螺杆菌感染可在小鼠和人类中诱导1型辅助性T细胞反应。通过用重组幽门螺杆菌脲酶B亚基（rUreB）进行黏膜免疫，可治愈小鼠或使其免受幽门螺杆菌感染。本研究对感染小鼠经rUreB免疫后的免疫反应进行了特征分析。
将BALB/c小鼠感染猫幽门螺杆菌。两周后，每周一次用rUreB和霍乱毒素（CT）对其进行4次口服免疫。对照组仅进行感染或用CT进行假免疫。免疫后在不同时间处死动物。获取脾CD4(+)细胞，并在体外与rUreB一起培养，以评估抗原特异性增殖以及干扰素γ和白细胞介素4分泌的诱导情况。
所有经rUreB免疫的小鼠（n = 8）在第四次免疫后3周感染被治愈。免疫诱导了脾CD4(+)细胞的增殖反应，每次免疫后干扰素γ分泌逐渐减少，同时白细胞介素4分泌增加。在感染/免疫的小鼠中观察到rUreB特异性血清免疫球蛋白G1水平同时升高。
在BALB/c小鼠中，用rUreB进行治疗性黏膜免疫逐渐诱导Th2 CD4(+) T细胞反应，从而导致病原体的清除。
