Hypertrophic gastropathy in Helicobacter felis - Infected wild-type C57BL/6 mice and p53 hemizygous transgenic mice
Hypertrophic gastropathy in Helicobacter felis - Infected wild-type C57BL/6 mice and p53 hemizygous transgenic mice
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DOI：
10.1053/gast.1996.v110.pm8536852
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发表时间：
1996-01-01
期刊：
影响因子：
29.4
通讯作者：
Wang, TC
中科院分区：
文献类型：
--
作者：
Fox, JG;Li, XT;Wang, TC
背景和目标：幽门螺杆菌（Helicobacter pylori，Hp）感染可引起胃炎和消化性溃疡，在流行病学上与胃癌有关。通过胃插管将猫感染SPF级C57 BL/6野生型和p53半合子小鼠，并随访1年，通过组织学、增殖细胞核抗原（PCNA）染色和5-溴-2 '-脱氧尿苷（BrdU）分析，与相同基因型的未感染对照组进行比较。感染六个月后，与未感染的对照组相比，野生型和p53半合子小鼠均表现出活跃的慢性炎症和明显的粘膜增生。感染H.野生型和p53半合子小鼠的视网膜表面小凹上皮细胞均呈严重的腺瘤样和囊性增生，BrdU摄取和PCNA染色均较对照组明显增加，p53半合子小鼠的增殖指数高于野生型小鼠。猫C57 BL/6基因型可诱导肥大性胃病;一个p53等位基因的缺失，尽管不足以在1年时启动致癌作用，但可增强增殖指数，这可能导致癌症诱导风险增加。
Background & Aims: Helicobacter pylori infection causes gastritis and peptic ulcers and is linked epidemiologically to gastric cancer, To analyze host genetic factors and the influence of Helicobacter on cell proliferation, we used an inbred and p53 hemizygous mouse model of Helicobacter felis-induced gastritis, Methods: H. felis was inoculated by gastric intubation into SPF C57BL/6 wild-type and p53 hemizygous mice that were followed up for 1 year and compared with uninfected controls of the same genotype using histology, proliferating cell nuclear antigen (PCNA) staining, and 5-bromo-2'-deoxyuridine (BrdU) analysis, Results: Infected animals developed sustained anti-H, felis serum immunoglobulin G antibody responses. Six months after infection, both wild-type and p53 hemizygous mice showed active chronic inflammation and marked mucosal hyperplasia compared with uninfected controls, One year after infection with H. felis, the wildtype and p53 hemizygous mice showed severe adenomatous and cystic hyperplasia of the surface foveolar epithelium, BrdU uptake and PCNA staining were markedly increased in both sets of infected mice compared with controls, Infected p53 hemizygous mice had a higher proliferative index than the infected wild-type mice, Conclusions: H. felis can induce a hypertrophic gastropathy in the C57BL/6 genotype; loss of one p53 allele, although insufficient to initiate carcinogenesis at 1 year, enhances the proliferative index, which may lead to an increased risk of cancer induction.