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首页> 外文期刊>Journal of gastroenterology and hepatology >Microcirculatory alteration in low-grade gastric mucosa-associated lymphoma by Helicobacter heilmannii infection: Its relation to vascular endothelial growth factor and cyclooxygenase-2
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Microcirculatory alteration in low-grade gastric mucosa-associated lymphoma by Helicobacter heilmannii infection: Its relation to vascular endothelial growth factor and cyclooxygenase-2

机译:Heilmannbacter heilmannii感染在低级胃黏膜相关淋巴瘤中的微循环改变:与血管内皮生长因子和环氧合酶-2的关系。

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Background: There are clinical reports that Helicobacter heilmannii, as well as Helicobacter pylori, has been clinically reported to cause gastric low-grade mucosa-associated lymphoid tissue-type (MALT) lymphoma, although its precise mechanism remains to be clarified. Thus, the present study was undertaken to elucidate the alteration of the microcirculatory structure and the relation to angiogenetic factors in mice infected with H. heilmannii for 3 and 6 months. Methods: Immunohistochemical studies have been performed by FITC-dextran intra-aortic infusion or CD31, vascular endothelial growth factor-A, cyclooxygenase 2 antibodies using our recently established model of gastric mucosa-associated lymphoid tissue-type gastric B-cell lymphoma in C57BL/6 mice. Results: Increased microcirculatory network was recognized surrounding the MALT lymphoma tissues by both the FITC-dextran infusion method and CD31 immunoreactivity. Vascular endothelial growth factor-A immunoreactivity was recognized within the lymphoma tissues as well as in the marginal area, while cyclooxygense-2 immunoreactivity was localized in the area surrounding the MALT lymphoma tissues. Conclusion: Increased microvascular network as well as enhanced VEGF-A immunoreactivity was shown to be related to expansion of the MALT lymphoma formed by Helicobacter heilmannii infection.
机译:背景:有临床报道称,临床已报道了Helibacter heilmannii和幽门螺杆菌(Helicobacter pylori)可引起胃低级粘膜相关淋巴样组织(MALT)淋巴瘤,尽管其确切机制尚待阐明。因此,进行本研究以阐明在感染海尔曼氏杆菌3个月和6个月的小鼠中微循环结构的改变以及与血管生成因子的关系。方法:采用我们最近建立的胃黏膜相关淋巴样组织型胃B细胞淋巴瘤模型,通过FITC-右旋糖酐主动脉内输注或CD31,血管内皮生长因子-A,环氧合酶2抗体进行了免疫组织化学研究。 6只小鼠。结果:FITC-葡聚糖输注法和CD31免疫反应性均能识别出MALT淋巴瘤组织周围微循环网络的增加。血管内皮生长因子-A免疫反应性被公认在淋巴瘤组织内以及边缘区域,而环氧合酶2免疫反应性则位于MALT淋巴瘤组织周围。结论:增加的微血管网络以及增强的VEGF-A免疫反应性与Helibacter heilmannii感染形成的MALT淋巴瘤的扩大有关。

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