幽门螺杆菌疫苗接种小鼠产生免疫后胃炎的影响因素

目的:研究幽门螺杆菌(H pylorl)疫苗接种小鼠产生免疫后胃炎的影响因素．方法:将H pylori疫苗免疫C57BL／6和BALB／c的小鼠,观察攻击后胃黏膜H pylori定植和炎症情况．将H pylori疫苗免疫C57BL／6小鼠,然后予不同菌量的H pylori攻击,观察胃黏膜H Pylori定植和炎症情况．将H pylori疫苗经口和经腹腔免疫C57BL／6小鼠,观察攻击后胃黏膜H pylori定植和炎症情况.对感染H pylori的C57BL／6小鼠予H pylori疫苗治疗,观察治疗免疫后胃黏膜H pylori定植和炎症情况．结果:不同品系的小鼠免疫保护程度无明显差异,但C57BL／6小鼠免疫后胃炎重于BALB／c小鼠．接受不同攻击茵量的小鼠保护程度无明显差异,但大的攻击茵量可诱导更严重的免疫后炎症．不同免疫途径诱导的免疫保护程度及攻击后不同时间点的炎症程度均无显著性差异．治疗性免疫导致H pylori定植明显降低,同时也引发更为严重的胃炎．结论:在不同的免疫宿主、免疫途径和治疗性免疫中均存在免疫后胃炎．免疫后胃炎的强弱程度受免疫宿主和攻击菌量的影响．

Influence factors of post-immunization gastritis after Helicobacter pylori vaccine immunization in mice

AIM: To explore the influence factors of post-immunization gastritis after H pylori vaccine immunization in mice. METHODS: (1) C57BL/6 and BALB/c mice were orally immunized with H pylori vaccine (H pylori whole cell sonicate antigen plus mucosa adjuvant cholera toxin). Gastric H pylori infection and inflammation were evaluated after H pylori challenge. (2) C57BL/6 mice were orally immunized with H pylori vaccine, and then challenged by different amounts of H pylori. Gastric H pylori infection and inflammation were evaluated after H pylori challenge. (3) C57BL/6 mice were immunized orally or intraperitoneally with H pylori vaccine. Gastric H pylori infection and inflammation were evaluated after H pylori challenge at different time points. (4) Infected C57BL/6 mice were orally immunized with H pylori vaccine, and gastric H pylori infection and inflammation were evaluated after immunization at different time points. RESULTS: (1) Similar decreasing of H pylori colonization was found in both C57BL/6 and BALB/c mice. However, C57BL/6 mice showed more severe post-immunization gastritis than BALB/c mice did. (2) Although H pylori colonization was similar in all groups with different challenging amounts, larger amount of H pylori challenge induced more severe post-immunization gastritis. (3) Similar post-immunization gastritis and decreasing of H pylori colonization were found in mice with both oral and intraperitoneal immunization at different time points. (4) Therapeutic immunization led to significant decreasing of H pylori colonization in infected mice; meanwhile more severe gastritis was also found in therapeutic group when compared with that in control group. CONCLUSION: Post-immunization gastritis occurs in different immune hosts, the same hosts with different vaccination routes and hosts received therapeutic immunization. H pylori challenge amounts and immune host are influential factors of post-immunization gastritis degree.