幽门螺杆菌是世界上至少一半人口的胃中的常见居民,最近的证据表明它出现在其他器官,如胰腺。在这个器官里,据报道,在猫中存在幽门螺杆菌DNA,尽管功能影响仍然未知。在这项工作中,我们在啮齿动物模型中确定了与胰腺中幽门螺杆菌表现相关的不同特征,以分析其功能和结构效应。接种幽门螺杆菌的沙鼠表现出这种细菌的存在,正如一些毒力因子的表达所揭示的那样,作为胃和胰腺中的CagA和OMPs,并由脲酶活性证实,细菌培养,PCR和免疫荧光测定。在感染动物的胰腺组织中观察到非明显的形态学变化;然而,细胞间连接蛋白的离域(claudin-1,claudin-4,occludin,ZO-1,E-钙粘蛋白,β-连环蛋白,显示了desmoglein-2和desmoplakinI/II)和肌动蛋白细胞骨架的重排。这种结构损伤与胰岛素和胰高血糖素分布的改变是一致的,和全身性炎症,事件表现为IL-8水平升高。总的来说,这些发现表明幽门螺杆菌可以到达胰腺,可能影响其功能并有助于胰腺疾病的发展。
Helicobacter pylori is a common resident in the stomach of at least half of the world\'s population and recent evidence suggest its emergence in other organs such as the pancreas. In this organ, the presence of H. pylori DNA has been reported in cats, although the functional implications remain unknown. In this work, we determined distinct features related to the H. pylori manifestation in pancreas in a rodent model, in order to analyse its functional and structural effect. Gerbils inoculated with H. pylori exhibited the presence of this bacterium, as revealed by the expression of some virulence factors, as CagA and OMPs in stomach and pancreas, and confirmed by urease activity, bacterial culture, PCR and immunofluorescence assays. Non-apparent morphological changes were observed in pancreatic tissue of infected animals; however, delocalization of intercellular junction proteins (claudin-1, claudin-4, occludin, ZO-1, E-cadherin, β-catenin, desmoglein-2 and desmoplakin I/II) and rearrangement of the actin-cytoskeleton were exhibited. This structural damage was consistent with alterations in the distribution of insulin and glucagon, and a systemic inflammation, event demonstrated by elevated IL-8 levels. Overall, these findings indicate that H. pylori can reach the pancreas, possibly affecting its function and contributing to the development of pancreatic diseases.