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- W4322742055 endingPage "651" @default.
- W4322742055 startingPage "651" @default.
- W4322742055 abstract "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." @default.
- W4322742055 created "2023-03-03" @default.
- W4322742055 creator A5024568665 @default.
- W4322742055 creator A5025592752 @default.
- W4322742055 creator A5037418339 @default.
- W4322742055 creator A5038754122 @default.
- W4322742055 creator A5078161597 @default.
- W4322742055 date "2023-02-28" @default.
- W4322742055 modified "2023-10-18" @default.
- W4322742055 title "IL-8 Secreted by Gastric Epithelial Cells Infected with Helicobacter pylori CagA Positive Strains Is a Chemoattractant for Epstein–Barr Virus Infected B Lymphocytes" @default.
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