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幽门螺杆菌感染对小鼠模型胃和脊髓神经元表达的作用。

Role of Helicobacter pylori infection on neuronal expression in the stomach and spinal cord of a murine model.

机构信息

Department of Gastroenterology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai Institute of Digestive Disease, Shanghai, China.

出版信息

J Dig Dis. 2009 Nov;10(4):286-92. doi: 10.1111/j.1751-2980.2009.00397.x.

DOI:10.1111/j.1751-2980.2009.00397.x
PMID:19906107
Abstract

OBJECTIVE

To investigate the effect of Helicobacter pylori (H. pylori) infection on neuronal expressions in the stomach and spinal cord of mice so as to explain dyspepsia symptoms in H. pylori infected patients.

METHODS

C57BL/6 female mice were studied at 2 weeks (acute infection group) and 12 weeks (chronic infection group) after H. pylori inoculation. Histological analyses for gastric inflammation and bacterial colonization were assessed by HE staining and Warthin-Starry staining. Fos, vasoactive intestinal polypeptide (VIP) and calcitonin gene-related peptide expressions (CGRP) were studied by immunohistochemistry.

RESULTS

H. pylori colonization was present mainly in pyloric region, but bacterial density was similar in both infected groups. The intensity of mucosal inflammation and activity was significantly higher in two infected groups than in those in the control group. The degree of mononuclear and polymorphonuclear cell infiltration in proventricular-glandular region and gastric corpus at 12 weeks after H. pylori inoculation was higher than that at 2 weeks after inoculation. The neuronal expressions of fos, VIP, and CGRP in the stomach and spinal cord were significantly more marked in the infected groups than in the control group, but there was no significant difference between two infected groups.

CONCLUSION

H. pylori infection induced different degrees of gastric mucosal inflammation in the murine model. Both early and chronic infection groups of mice showed enhanced neuronal expressions of fos, VIP and CGRP of stomach and spinal cord and these could form a basis for appearance of functional dyspeptic symptoms in patients with H. pylori infection.

摘要

目的

研究幽门螺杆菌(H. pylori)感染对小鼠胃和脊髓神经元表达的影响,从而解释 H. pylori 感染患者的消化不良症状。

方法

在 H. pylori 接种后 2 周(急性感染组)和 12 周(慢性感染组),对 C57BL/6 雌性小鼠进行研究。通过 HE 染色和 Warthin-Starry 染色评估胃炎症和细菌定植的组织学分析。通过免疫组织化学研究 Fos、血管活性肠肽(VIP)和降钙素基因相关肽(CGRP)的表达。

结果

H. pylori 定植主要发生在幽门区,但两组感染小鼠的细菌密度相似。两组感染小鼠的黏膜炎症和活性强度明显高于对照组。与接种后 2 周相比,接种后 12 周幽门腺区和胃体的单核细胞和多形核细胞浸润程度更高。感染组胃和脊髓神经元中 fos、VIP 和 CGRP 的表达明显高于对照组,但两组感染组之间无显著差异。

结论

H. pylori 感染在小鼠模型中引起不同程度的胃黏膜炎症。在感染的早期和慢性感染组中,小鼠胃和脊髓神经元中 fos、VIP 和 CGRP 的表达增强,这可能是 H. pylori 感染患者出现功能性消化不良症状的基础。

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