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目的研究幽门螺杆菌(Hp)感染对小鼠胃和脊髓神经元表达的影响,探讨Hp感染产生消化不良症状的可能机制。方法建立Hp感染小鼠模型,35只雌性C57BL/6小鼠分为3组急性感染组(感染后2周组,15只)和慢性感染组(感染后12周组,15只),并以生理盐水灌胃的小鼠作为对照(对照组,5只)。小鼠胃黏膜经HE染色和Warthin-Starry染色评估组织学改变和Hp定植密度,经免疫组织化学染色评估胃和脊髓Fos、血管活性肠肽(VIP)及降钙素基因相关肽(CGRP)阳性神经元,并进行比较。结果Hp感染12周时3只小鼠死亡,Hp定植密度明显高于感染2周时,且主要分布在幽门腺黏膜。感染后2周和12周组小鼠幽门腺区、前胃-腺胃交界区及胃体腺区炎症和活动性水平均明显高于对照组,且以感染12周组为重。小鼠胃和脊髓Fos、VIP及CGRP神经元阳性程度(积分)在Hp感染后2周组(15只,分别为胃3.1±1.4、4.5±1.8和2.4±0.8,脊髓3.8±1.2、3.2±1.5和2.2±0.6)和感染后12周组(12只,分别为胃3.1±1.3、3.5±1.6和2.2±0.8;脊髓3.4±0.7、2.6±1.2和2.5±1.1)差异无统计学意义(均P>0.05),但均显著高于对照组(5只,分别为胃2.4±0.9、1.6±0.9和1.2±0.8,脊髓2.0±1.6、1.2±1.1和1.2±1.1,均P<0.05)。结论急性和慢性Hp感染引起小鼠胃黏膜不同程度炎症和活动性等组织学改变,并有胃和脊髓Fos、VIP及CGRP阳性神经元表达显著增加,这可能是Hp阳性消化不良患者症状产生的基础。
Objective To investigate the effect of Helicobacter pylori (Hp) infection on the expression of neurons in the stomach and spinal cord of mice and to explore the possible mechanism of dyspeptic symptoms caused by Hp infection. Methods The mouse model of Hp infection was established. 35 female C57BL / 6 mice were divided into 3 groups: acute infection group (2 weeks after infection, 15 animals) and chronic infection group (12 weeks after infection, 15 animals) Saline gavage mice as a control (control group, 5). Histological changes and Hp colonization density of gastric mucosa of mice were evaluated by HE staining and Warthin-Starry staining. Fos, VIP and CGRP in stomach and spinal cord were evaluated by immunohistochemical staining Neurons, and compare. Results Three mice died at the 12th week of Hp infection. The density of Hp colonization was significantly higher than that of 2 weeks after infection, and mainly distributed in the pyloric gland mucosa. The levels of inflammation and activity in the pyloric gland, anterior gastric-gastral junction and corpus gland of 2 and 12 weeks after infection were significantly higher than those in the control group, and the 12 weeks of infection was the most important. The positive degree (integral) of Fos, VIP and CGRP neurons in the stomach and spinal cord of mice were observed in the two weeks after Hp infection (15, 3.1 ± 1.4, 4.5 ± 1.8 and 2.4 ± 0.8, 3.8 ± 1.2 and 3.2 ± 1.5 and 2.2 ± 0.6) and 12 weeks post infection (12, 3.1 ± 1.3, 3.5 ± 1.6 and 2.2 ± 0.8, respectively; 3.4 ± 0.7, 2.6 ± 1.2 and 2.5 ± 1.1, respectively) (All P> 0.05), but all were significantly higher than those in the control group (5, 2.4 ± 0.9, 1.6 ± 0.9 and 1.2 ± 0.8, 2.0 ± 1.6, 1.2 ± 1.1 and 1.2 ± 1.1, respectively, P <0.05) . Conclusions Acute and chronic H. pylori infection cause histological changes of gastric mucosa in mice, such as inflammation and activity, and the expression of Fos, VIP and CGRP positive neurons in stomach and spinal cord are significantly increased, which may be caused by the symptoms of Hp positive dyspepsia patients basis.