Aristoteli Lina Panayiota, O'Rourke Jani L, Danon Stephen, Larsson Hakan, Mellgard Bjorn, Mitchell Hazel, Lee Adrian
School of Biotechnology and Biomolecular Science, University of New South Wales, Sydney, NSW, Australia.
Helicobacter. 2006 Oct;11(5):460-8. doi: 10.1111/j.1523-5378.2006.00439.x.
Helicobacter pylori is a causative agent of gastric and duodenal ulcers and gastric cancer. Its urease enzyme allows survival in acid conditions and drives bacterial intracellular metabolism. We aimed to investigate the role of urease in determining the intragastric distribution of Helicobacter species in vivo.
The C57BL/6 mouse model of gastritis was used for infection with Helicobacter felis (CS1) or H. pylori (SS1). Urease-modulating compounds urea and/or fluorofamide (urease inhibitor) were administered to mice over 7 days. Concurrent gastric acid inhibition by omeprazole was also examined. Bacterial distribution in the antrum, body, antrum/body, and body/cardia transitional zones was graded "blindly" by histologic evaluation. Bacterial colony counts on corresponding tissue were also conducted.
Urease inhibition by fluorofamide decreased H. pylori survival in most gastric regions (p < .05); however, there were no marked changes to H. felis colonization after this treatment. There was a consistent trend for decreased antral colonization, and an increase in antrum/body transitional zone and body colonization with excess 5% or 6% (w/v) urea treatment. Significant reductions of both Helicobacter species were observed with the co-treatment of urea and fluorofamide (p < .05). Collateral treatment with omeprazole did not alter H. pylori colonization patterns caused by urea/fluorofamide.
Urease perturbations affect colonization patterns of Helicobacter species. Combined urea and fluorofamide treatment reduced the density of both Helicobacter species in our infection model.
幽门螺杆菌是胃和十二指肠溃疡以及胃癌的病原体。其脲酶可使其在酸性环境中存活并驱动细菌的细胞内代谢。我们旨在研究脲酶在确定幽门螺杆菌在体内胃内分布中的作用。
采用C57BL/6小鼠胃炎模型感染猫幽门螺杆菌（CS1）或幽门螺杆菌（SS1）。在7天内给小鼠施用脲酶调节化合物尿素和/或氟甲酰胺（脲酶抑制剂）。还检测了奥美拉唑同时抑制胃酸的情况。通过组织学评估“盲目”分级胃窦、胃体、胃窦/胃体和胃体/贲门过渡区的细菌分布。还对相应组织进行了细菌菌落计数。
氟甲酰胺抑制脲酶降低了幽门螺杆菌在大多数胃区域的存活率（p < 0.05）；然而，该处理后猫幽门螺杆菌的定植没有明显变化。5%或6%（w/v）过量尿素处理后，胃窦定植减少，胃窦/胃体过渡区和胃体定植增加的趋势一致。尿素和氟甲酰胺联合处理观察到两种幽门螺杆菌均显著减少（p < 0.05）。奥美拉唑辅助治疗未改变尿素/氟甲酰胺引起的幽门螺杆菌定植模式。
脲酶扰动影响幽门螺杆菌的定植模式。在我们的感染模型中，尿素和氟甲酰胺联合处理降低了两种幽门螺杆菌的密度。
