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Helicobacter suis causes severe gastric pathology in mouse and Mongolian gerbil models of human gastric disease

机译:在人胃病的小鼠和蒙古沙鼠模型中,幽门螺杆菌引起严重的胃病理学

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摘要

Background: “Helicobacter (H.) heilmannii” type 1 is the most prevalent gastric non-H. pylori Helicobacter species in humans suffering from gastric disease. It has been shown to be identical to H. suis, a bacterium which is mainly associated with pigs. To obtain better insights into the long-term pathogenesis of infections with this micro-organism, experimental infections were carried out in different rodent models. Methodology/Principal findings: Mongolian gerbils and mice of two strains (BALB/c and C57BL/6) were infected with H. suis and sacrificed at 3 weeks, 9 weeks and 8 months after infection. Gastric tissue samples were collected for PCR analysis, histological and ultrastructural examination. In gerbils, bacteria mainly colonized the antrum and a narrow zone in the fundus near the forestomach/stomach transition zone. In both mice strains, bacteria colonized the entire glandular stomach. Colonization with H. suis was associated with necrosis of parietal cells in all three animal strains. From 9 weeks after infection onwards, an increased proliferation rate of mucosal epithelial cells was detected in the stomach regions colonized with H. suis. Most gerbils showed a marked lymphocytic infiltration in the antrum and in the forestomach/stomach transition zone, becoming more pronounced in the course of time. At 8 months post infection, severe destruction of the normal antral architecture at the inflamed sites and development of mucosa-associated lymphoid tissue (MALT) lymphoma-like lesions were observed in some gerbils. In mice, the inflammatory response was less pronounced than in gerbils, consisting mainly of mononuclear cell infiltration and being most severe in the fundus. Conclusions/Significance: H. suis causes death of parietal cells, epithelial cell hyperproliferation and severe inflammation in mice and Mongolian gerbil models of human gastric disease. Moreover, MALT lymphoma-like lesions were induced in H. suis-infected Mongolian gerbils. Therefore, the possible involvement of this micro-organism in human gastric disease should not be neglected.
机译:背景:“ Helicobacter(H.)heilmannii” 1型是最普遍的胃部非H胃病。患有胃病的人类中的幽门螺杆菌。它已显示出与猪嗜血杆菌相同,后者主要与猪有关。为了更好地了解这种微生物感染的长期发病机理,在不同的啮齿动物模型中进行了实验性感染。方法/主要发现:蒙古沙鼠和两种品系(BALB / c和C57BL / 6)的小鼠感染了猪链球菌,并在感染后3周,9周和8个月处死。收集胃组织样品用于PCR分析,组织学和超微结构检查。在沙鼠中,细菌主要定居在胃窦/胃过渡区附近的胃窦和眼底狭窄区。在这两种小鼠品系中,细菌都定居在整个腺胃中。在所有三种动物品系中,猪嗜血杆菌的定殖与壁细胞坏死有关。从感染后9周开始,在猪嗜血杆菌定植的胃区域中检测到粘膜上皮细胞的增殖速率增加。大多数沙鼠在胃窦和前胃/胃过渡区都显示出明显的淋巴细胞浸润,随着时间的流逝变得更加明显。感染后8个月,在一些沙鼠中观察到发炎部位正常的肛门结构遭到严重破坏,并出现了粘膜相关淋巴样组织(MALT)淋巴瘤样病变的发展。在小鼠中,炎症反应没有沙鼠那么明显,主要由单核细胞浸润组成,并且在眼底最严重。结论/意义:猪链球菌可引起小鼠和蒙古沙土鼠人胃病模型的壁细胞死亡,上皮细胞过度增殖和严重炎症。此外,在感染了猪链球菌的蒙古沙鼠中诱发了MALT淋巴瘤样病变。因此,不应忽略这种微生物与人胃病的关系。

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