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小鼠模型中幽门螺杆菌诱导胃淋巴瘤发生过程中炎症反应的特征分析

Characterisation of inflammatory processes in Helicobacter pylori-induced gastric lymphomagenesis in a mouse model.

作者信息

Floch Pauline, Laur Amandine Marine, Korolik Victoria, Chrisment Delphine, Cappellen David, Idrissi Yamina, Dubus Pierre, Mégraud Francis, Lehours Philippe

机构信息

University of Bordeaux, Bacteriology Laboratory, Bordeaux, France.

Inserm U853, Bordeaux, France.

出版信息

Oncotarget. 2015 Oct 27;6(33):34525-36. doi: 10.18632/oncotarget.5948.

DOI:10.18632/oncotarget.5948
PMID:26439692
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4741470/
Abstract

Gastric MALT lymphoma (GML) can be induced by Helicobacter pylori infection in BALB/c mice thymectomised at day 3 post-birth (d3Tx). This represented a unique opportunity to investigate the inflammatory process involved in the recruitment, proliferation and structuration of lymphoid infiltrates in the gastric mucosa of mice developing GML. Complementary molecular and proteomic approaches demonstrated that Th1 and Th2 cytokines were upregulated, along with activators/regulators of the lymphoid response and numerous chemokines. Interleukin-4, interferon γ, lymphotoxin-α and -β were significantly upregulated and correlated with the inflammatory scores for all the d3Tx mice. GML lesions in d3Tx mice infected with H. pylori were associated with the presence of the inflammatory response. The dysregulation of numerous members of the tumour necrosis factor superfamily was also evident and suggests that they could play an important role in GML pathology, especially in light of their ability to promote and control lymphocyte proliferation.

摘要

胃黏膜相关淋巴组织淋巴瘤(GML)可由出生后第3天进行胸腺切除(d3Tx)的BALB/c小鼠中的幽门螺杆菌感染诱导产生。这为研究GML发生过程中小鼠胃黏膜中淋巴浸润的募集、增殖和结构形成所涉及的炎症过程提供了一个独特的机会。互补的分子和蛋白质组学方法表明,Th1和Th2细胞因子以及淋巴样反应的激活剂/调节剂和众多趋化因子均上调。白细胞介素-4、干扰素γ、淋巴毒素-α和-β显著上调,并与所有d3Tx小鼠的炎症评分相关。感染幽门螺杆菌的d3Tx小鼠中的GML病变与炎症反应的存在有关。肿瘤坏死因子超家族众多成员的失调也很明显,这表明它们可能在GML病理学中发挥重要作用,特别是鉴于它们促进和控制淋巴细胞增殖的能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8546/4741470/03200b970342/oncotarget-06-34525-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8546/4741470/75957b4c7ae8/oncotarget-06-34525-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8546/4741470/23635ebf7117/oncotarget-06-34525-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8546/4741470/5087c6e5c294/oncotarget-06-34525-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8546/4741470/03200b970342/oncotarget-06-34525-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8546/4741470/75957b4c7ae8/oncotarget-06-34525-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8546/4741470/23635ebf7117/oncotarget-06-34525-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8546/4741470/5087c6e5c294/oncotarget-06-34525-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8546/4741470/03200b970342/oncotarget-06-34525-g004.jpg

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