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Helicobacter pylori Disrupts Host Cell Membranes, Initiating a Repair Response and Cell Proliferation

Helicobacter pylori (H. pylori), the human stomach pathogen, lives on the inner surface of the stomach and causes chronic gastritis, peptic ulcer, and gastric cancer. Plasma membrane repair response is a matter of life and death for human cells against physical and biological damage. We here test th...

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Autores principales: Lin, Li-Ling, Huang, Hsuan-Cheng, Ogihara, Satoshi, Wang, Jin-Town, Wu, Meng-Chuan, McNeil, Paul L., Chen, Chiung-Nien, Juan, Hsueh-Fen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Molecular Diversity Preservation International (MDPI) 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3431852/
https://www.ncbi.nlm.nih.gov/pubmed/22949854
http://dx.doi.org/10.3390/ijms130810176
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author Lin, Li-Ling
Huang, Hsuan-Cheng
Ogihara, Satoshi
Wang, Jin-Town
Wu, Meng-Chuan
McNeil, Paul L.
Chen, Chiung-Nien
Juan, Hsueh-Fen
author_facet Lin, Li-Ling
Huang, Hsuan-Cheng
Ogihara, Satoshi
Wang, Jin-Town
Wu, Meng-Chuan
McNeil, Paul L.
Chen, Chiung-Nien
Juan, Hsueh-Fen
author_sort Lin, Li-Ling
collection PubMed
description Helicobacter pylori (H. pylori), the human stomach pathogen, lives on the inner surface of the stomach and causes chronic gastritis, peptic ulcer, and gastric cancer. Plasma membrane repair response is a matter of life and death for human cells against physical and biological damage. We here test the hypothesis that H. pylori also causes plasma membrane disruption injury, and that not only a membrane repair response but also a cell proliferation response are thereby activated. Vacuolating cytotoxin A (VacA) and cytotoxin-associated gene A (CagA) have been considered to be major H. pylori virulence factors. Gastric cancer cells were infected with H. pylori wild type (vacA+/cagA+), single mutant (ΔvacA or ΔcagA) or double mutant (ΔvacA/ΔcagA) strains and plasma membrane disruption events and consequent activation of membrane repair components monitored. H. pylori disrupts the host cell plasma membrane, allowing localized dye and extracellular Ca(2+) influx. Ca(2+)-triggered members of the annexin family, A1 and A4, translocate, in response to injury, to the plasma membrane, and cell surface expression of an exocytotic maker of repair, LAMP-2, increases. Additional forms of plasma membrane disruption, unrelated to H. pylori exposure, also promote host cell proliferation. We propose that H. pylori activation of a plasma membrane repair is pro-proliferative. This study might therefore provide new insight into potential mechanisms of H. pylori-induced gastric carcinogenesis.
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spelling pubmed-34318522012-09-04 Helicobacter pylori Disrupts Host Cell Membranes, Initiating a Repair Response and Cell Proliferation Lin, Li-Ling Huang, Hsuan-Cheng Ogihara, Satoshi Wang, Jin-Town Wu, Meng-Chuan McNeil, Paul L. Chen, Chiung-Nien Juan, Hsueh-Fen Int J Mol Sci Article Helicobacter pylori (H. pylori), the human stomach pathogen, lives on the inner surface of the stomach and causes chronic gastritis, peptic ulcer, and gastric cancer. Plasma membrane repair response is a matter of life and death for human cells against physical and biological damage. We here test the hypothesis that H. pylori also causes plasma membrane disruption injury, and that not only a membrane repair response but also a cell proliferation response are thereby activated. Vacuolating cytotoxin A (VacA) and cytotoxin-associated gene A (CagA) have been considered to be major H. pylori virulence factors. Gastric cancer cells were infected with H. pylori wild type (vacA+/cagA+), single mutant (ΔvacA or ΔcagA) or double mutant (ΔvacA/ΔcagA) strains and plasma membrane disruption events and consequent activation of membrane repair components monitored. H. pylori disrupts the host cell plasma membrane, allowing localized dye and extracellular Ca(2+) influx. Ca(2+)-triggered members of the annexin family, A1 and A4, translocate, in response to injury, to the plasma membrane, and cell surface expression of an exocytotic maker of repair, LAMP-2, increases. Additional forms of plasma membrane disruption, unrelated to H. pylori exposure, also promote host cell proliferation. We propose that H. pylori activation of a plasma membrane repair is pro-proliferative. This study might therefore provide new insight into potential mechanisms of H. pylori-induced gastric carcinogenesis. Molecular Diversity Preservation International (MDPI) 2012-08-15 /pmc/articles/PMC3431852/ /pubmed/22949854 http://dx.doi.org/10.3390/ijms130810176 Text en © 2012 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0 This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Article
Lin, Li-Ling
Huang, Hsuan-Cheng
Ogihara, Satoshi
Wang, Jin-Town
Wu, Meng-Chuan
McNeil, Paul L.
Chen, Chiung-Nien
Juan, Hsueh-Fen
Helicobacter pylori Disrupts Host Cell Membranes, Initiating a Repair Response and Cell Proliferation
title Helicobacter pylori Disrupts Host Cell Membranes, Initiating a Repair Response and Cell Proliferation
title_full Helicobacter pylori Disrupts Host Cell Membranes, Initiating a Repair Response and Cell Proliferation
title_fullStr Helicobacter pylori Disrupts Host Cell Membranes, Initiating a Repair Response and Cell Proliferation
title_full_unstemmed Helicobacter pylori Disrupts Host Cell Membranes, Initiating a Repair Response and Cell Proliferation
title_short Helicobacter pylori Disrupts Host Cell Membranes, Initiating a Repair Response and Cell Proliferation
title_sort helicobacter pylori disrupts host cell membranes, initiating a repair response and cell proliferation
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3431852/
https://www.ncbi.nlm.nih.gov/pubmed/22949854
http://dx.doi.org/10.3390/ijms130810176
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