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IL-8 Secreted by Gastric Epithelial Cells Infected with Helicobacter pylori CagA Positive Strains Is a Chemoattractant for Epstein–Barr Virus Infected B Lymphocytes

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...

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Autores principales: Domínguez-Martínez, Diana A., Fontes-Lemus, José I., García-Regalado, Alejandro, Juárez-Flores, Ángel, Fuentes-Pananá, Ezequiel M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10054738/
https://www.ncbi.nlm.nih.gov/pubmed/36992360
http://dx.doi.org/10.3390/v15030651
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author Domínguez-Martínez, Diana A.
Fontes-Lemus, José I.
García-Regalado, Alejandro
Juárez-Flores, Ángel
Fuentes-Pananá, Ezequiel M.
author_facet Domínguez-Martínez, Diana A.
Fontes-Lemus, José I.
García-Regalado, Alejandro
Juárez-Flores, Ángel
Fuentes-Pananá, Ezequiel M.
author_sort Domínguez-Martínez, Diana A.
collection PubMed
description 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.
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spelling pubmed-100547382023-03-30 IL-8 Secreted by Gastric Epithelial Cells Infected with Helicobacter pylori CagA Positive Strains Is a Chemoattractant for Epstein–Barr Virus Infected B Lymphocytes Domínguez-Martínez, Diana A. Fontes-Lemus, José I. García-Regalado, Alejandro Juárez-Flores, Ángel Fuentes-Pananá, Ezequiel M. Viruses Article 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. MDPI 2023-02-28 /pmc/articles/PMC10054738/ /pubmed/36992360 http://dx.doi.org/10.3390/v15030651 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Domínguez-Martínez, Diana A.
Fontes-Lemus, José I.
García-Regalado, Alejandro
Juárez-Flores, Ángel
Fuentes-Pananá, Ezequiel M.
IL-8 Secreted by Gastric Epithelial Cells Infected with Helicobacter pylori CagA Positive Strains Is a Chemoattractant for Epstein–Barr Virus Infected B Lymphocytes
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
title_full IL-8 Secreted by Gastric Epithelial Cells Infected with Helicobacter pylori CagA Positive Strains Is a Chemoattractant for Epstein–Barr Virus Infected B Lymphocytes
title_fullStr IL-8 Secreted by Gastric Epithelial Cells Infected with Helicobacter pylori CagA Positive Strains Is a Chemoattractant for Epstein–Barr Virus Infected B Lymphocytes
title_full_unstemmed IL-8 Secreted by Gastric Epithelial Cells Infected with Helicobacter pylori CagA Positive Strains Is a Chemoattractant for Epstein–Barr Virus Infected B Lymphocytes
title_short IL-8 Secreted by Gastric Epithelial Cells Infected with Helicobacter pylori CagA Positive Strains Is a Chemoattractant for Epstein–Barr Virus Infected B Lymphocytes
title_sort il-8 secreted by gastric epithelial cells infected with helicobacter pylori caga positive strains is a chemoattractant for epstein–barr virus infected b lymphocytes
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10054738/
https://www.ncbi.nlm.nih.gov/pubmed/36992360
http://dx.doi.org/10.3390/v15030651
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