幽门螺杆菌长期感染大鼠腺胃模型的建立

DEVELOPMENT OF WISTAR RAT MODEL OF HELECOBACTER PYLORI INFECTION

幽门螺杆菌HP）的致病机理仍不明确，动物实验有可能阐明其致病作用。目前尚无理想的人HP感染的动物模型。为此，我们用HP菌株（SyndeyStrain1，SS1）感染Wistar大鼠腺胃，以建立HP感染的大鼠模型。方法取二级Wistar大鼠40只，动物随机分为实验组（20只）及对照组（20只）。实验组动物接种HP菌液，大鼠1．5ml／只（约109／ml），连续5次，一周完成，而对照组则不作相应处理。距最后一次接种Hp的4、8、12、及24周分别处死实验组及对照组动物各5只。取动物胃粘膜组织分别进行尿素酶试验、HP培养、Gimesa染色及HE染色来评价SS1在Wistar大鼠腺胃的定植及病理组织学改变。结果4周时所有实验组动物胃窦、胃体HP检查均阳性，SS1主要定值于胃窦的胃小凹及腺腔，胃体较少且其定植量随感染时间的延长有增加的趋势，至24周时仍有明显定植；对照组功物未有HP定植。病理组织学检查，4周时动物未见炎症反应，至8周、12周和24周胃窦及胃体出现轻至中度慢性活动性胃炎，在本实验周期内未见萎缩性炎症改变，对照组动物无炎症反应。结论本研究表明SSIHP可长期定植于Wistar大鼠腺胃，引起慢性活动性胃炎，该模型的建立对于HP药物筛选、HP疫苗的研究及HP致病性的阐明具有重要的应用价值。

Aim To develop rat model of H. Pylon infection as to meet different requirement fordiffer ent purpose of study. Methods 40 two-grade Wistar rats were randomly divided into two groups,namelyexperi mental and control group,Anirnal in the experiment were inoculated orally Hp strain(Sydney Strain 1, SSl ), 1.5ml of inoculum per rat (10~9 organisms/ml) five times for a week. In 4, 8, 12 and 24 weeks after the last bacteriainoculum, 5 animals in the experiment and control were sacrificed respectively. Histology and HP colonizationwere assessed by HE sraining .Girnesa staining,Urease test and HP culture. Results in 4 week in allexperimen tal animals bacteria were deally visible at antrum and body, but the number of HP colonization in Wistar tendedto increase over the experiment time, HP were negative in the control. All animals had no inflammatory changesin 4 week,however, in 8, 12 and 24 weeks of the experiment,mild to moderate chronic active gastritis wasobsev ered in antrum and body,which increased in seventy over time, atrophy gastritis was still not seen in 24 weeks.In contrast, in the control, no remarkable changes were detected. Conclusions SS1 HP could colonize in theglandular stomach mucosa of Wistar rats and leaded to chronic active gastritis in long term study;SS1 rat modelwas adaptable for animal experimentation of HP including vaccine studies, screeing for novel therapeutics andin-vestigation of mechanisms of pathogenesis.