期刊
VIRUSES-BASEL
卷 15, 期 3, 页码 -出版社
MDPI
DOI: 10.3390/v15030651
关键词
Epstein-Barr virus (EBV); Helicobacter pylori (H; pylori); CagA; chemoattraction; IL-8; CXCR1; CXCR2; B lymphocytes
类别
Helicobacter pylori and EBV are major risk factors for gastric cancer, and both can establish persistent infections and are considered carcinogenic. The study suggests that Helicobacter pylori infection facilitates the chemoattraction of EBV-infected B lymphocytes to the gastric mucosa, with IL-8 being identified as a powerful chemoattractant and CXCR2 as the main IL-8 receptor induced by EBV. Inhibition of IL-8 and CXCR2 reduces the chemoattraction of EBV-infected B lymphocytes, indicating an interaction mechanism between Helicobacter pylori and EBV.
Helicobacter pylori and EBV are considered the main risk factors in developing gastric cancer. Both pathogens establish life-lasting infections and both are considered carcinogenic in humans. Different lines of evidence support that both pathogens cooperate to damage the gastric mucosa. Helicobacter pylori CagA positive virulent strains induce the gastric epithelial cells to secrete IL-8, which is a potent chemoattractant for neutrophils and one of the most important chemokines for the bacterium-induced chronic gastric inflammation. EBV is a lymphotropic virus that persists in memory B cells. The mechanism by which EBV reaches, infects and persists in the gastric epithelium is not presently understood. In this study, we assessed whether Helicobacter pylori infection would facilitate the chemoattraction of EBV-infected B lymphocytes. We identified IL-8 as a powerful chemoattractant for EBV-infected B lymphocytes, and CXCR2 as the main IL-8 receptor whose expression is induced by the EBV in infected B lymphocytes. The inhibition of expression and/or function of IL-8 and CXCR2 reduced the ERK1/2 and p38 MAPK signaling and the chemoattraction of EBV-infected B lymphocytes. We propose that IL-8 at least partially explains the arrival of EBV-infected B lymphocytes to the gastric mucosa, and that this illustrates a mechanism of interaction between Helicobacter pylori and EBV.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据