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IL-22 negatively regulates Helicobacter pylori-induced CCL20 expression in gastric epithelial cells.白细胞介素-22负向调节幽门螺杆菌诱导的胃上皮细胞中CCL20的表达。
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本文引用的文献

1
CCL28 is increased in human Helicobacter pylori-induced gastritis and mediates recruitment of gastric immunoglobulin A-secreting cells.CCL28在人幽门螺杆菌诱导的胃炎中增加,并介导胃免疫球蛋白A分泌细胞的募集。
Infect Immun. 2008 Jul;76(7):3304-11. doi: 10.1128/IAI.00041-08. Epub 2008 Apr 21.
2
Helicobacter pylori induces CCL20 expression.幽门螺杆菌诱导CCL20表达。
Infect Immun. 2007 Nov;75(11):5223-32. doi: 10.1128/IAI.00731-07. Epub 2007 Aug 27.
3
Upregulation of CCL20 and recruitment of CCR6+ gastric infiltrating lymphocytes in Helicobacter pylori gastritis.幽门螺杆菌胃炎中CCL20的上调及CCR6⁺胃浸润淋巴细胞的募集
Infect Immun. 2007 Sep;75(9):4357-63. doi: 10.1128/IAI.01660-06. Epub 2007 Jun 11.
4
Dendritic cells express CCR7 and migrate in response to CCL19 (MIP-3beta) after exposure to Helicobacter pylori.树突状细胞表达CCR7,并在暴露于幽门螺杆菌后对CCL19(MIP-3β)作出反应而迁移。
Microbes Infect. 2006 Mar;8(3):841-50. doi: 10.1016/j.micinf.2005.10.007. Epub 2006 Jan 13.
5
Increased number of mature dendritic cells in Crohn's disease: evidence for a chemokine mediated retention mechanism.克罗恩病中成熟树突状细胞数量增加:趋化因子介导的滞留机制的证据
Gut. 2006 Feb;55(2):220-7. doi: 10.1136/gut.2004.063008. Epub 2005 Aug 23.
6
Impact of Helicobacter pylori infection on gastric and plasma ghrelin dynamics in humans.幽门螺杆菌感染对人体胃及血浆胃饥饿素动态变化的影响。
Am J Gastroenterol. 2005 Aug;100(8):1711-20. doi: 10.1111/j.1572-0241.2005.41492.x.
7
Regulation of interleukin-6 promoter activation in gastric epithelial cells infected with Helicobacter pylori.幽门螺杆菌感染的胃上皮细胞中白细胞介素-6启动子激活的调控
Mol Biol Cell. 2005 Oct;16(10):4954-66. doi: 10.1091/mbc.e05-05-0426. Epub 2005 Jul 19.
8
Increased expression of CCL20 in human inflammatory bowel disease.CCL20在人类炎症性肠病中的表达增加。
J Clin Immunol. 2004 Jan;24(1):74-85. doi: 10.1023/B:JOCI.0000018066.46279.6b.
9
Helicobacter pylori persistence: biology and disease.幽门螺杆菌的持续存在:生物学与疾病
J Clin Invest. 2004 Feb;113(3):321-33. doi: 10.1172/JCI20925.
10
Involvement of myeloid dendritic cells in the development of gastric secondary lymphoid follicles in Helicobacter pylori-infected neonatally thymectomized BALB/c mice.髓样树突状细胞在新生期胸腺切除的幽门螺杆菌感染BALB/c小鼠胃次级淋巴滤泡发育中的作用
Infect Immun. 2003 Apr;71(4):2153-62. doi: 10.1128/IAI.71.4.2153-2162.2003.

CCL20在人幽门螺杆菌相关性胃炎中的表达增强。

Enhanced expression of CCL20 in human Helicobacter pylori-associated gastritis.

作者信息

Yoshida Akira, Isomoto Hajime, Hisatsune Junzo, Nakayama Masaaki, Nakashima Yujiro, Matsushima Kayoko, Mizuta Yohei, Hayashi Tomayoshi, Yamaoka Yoshio, Azuma Takeshi, Moss Joel, Hirayama Toshiya, Kohno Shigeru

机构信息

Second Department of Internal Medicine, Nagasaki University School of Medicine, Sakamoto, Nagasaki 852-8501, Japan.

出版信息

Clin Immunol. 2009 Mar;130(3):290-7. doi: 10.1016/j.clim.2008.09.016. Epub 2008 Nov 8.

DOI:10.1016/j.clim.2008.09.016
PMID:19006683
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3404125/
Abstract

CC chemokine ligand 20 (CCL20) attracts CC chemokine receptor 6 (CCR6)-expressing cells. Using endoscopic biopsies taken from the gastric antrum of 42 subjects infected with H. pylori and 42 uninfected subjects, mucosal CCL20 mRNA and protein levels were measured by real-time polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. CCL19 mRNA and protein levels, as well as CCL21 mRNA levels, were also measured. The CCL20 mRNA and protein levels were significantly elevated in H. pylori-positive patients and substantially decreased after successful eradication. CCL19 and CCL21 expression levels were comparable in the H. pylori-infected and the uninfected groups. The CCL20 concentrations correlated with the degree of chronic gastritis. Immunohistochemistry and the in vitro infection assay showed that CCL20 was principally produced by the gastric epithelium. CCR6-expressing cells, including CD45RO(+) memory T lymphocytes and fascin(+)-CD1a(+) immature dendritic cells, infiltrated close to the CCL20-expressing epithelial cells. The CCL20/CCR6 interaction may be involved in the development of H. pylori-associated gastritis.

摘要

C-C趋化因子配体20(CCL20)可吸引表达C-C趋化因子受体6(CCR6)的细胞。利用42名幽门螺杆菌感染受试者和42名未感染受试者的胃窦内镜活检样本,分别通过实时聚合酶链反应和酶联免疫吸附测定法检测黏膜CCL20 mRNA和蛋白水平。同时也检测了CCL19 mRNA和蛋白水平以及CCL21 mRNA水平。幽门螺杆菌阳性患者的CCL20 mRNA和蛋白水平显著升高,成功根除幽门螺杆菌后大幅下降。CCL19和CCL21的表达水平在幽门螺杆菌感染组和未感染组中相当。CCL20浓度与慢性胃炎程度相关。免疫组织化学和体外感染试验表明,CCL20主要由胃上皮细胞产生。表达CCR6的细胞,包括CD45RO(+)记忆T淋巴细胞和fascin(+)-CD1a(+)未成熟树突状细胞,浸润至表达CCL20的上皮细胞附近。CCL20/CCR6相互作用可能参与幽门螺杆菌相关性胃炎的发生发展。