Mechanisms of interacting <i>Helicobacter pylori</i> with gastric mucosal epithelium. II. A reaction of gastric epithelium on <i>Helicobacter pylori</i> colonization and persistence

Gastric and duodenal recurrent inflammatory diseases have a high prevalence, but the role played by microbes in its development remained unclear. However, the data published in 1983 by Marshall and Warren about isolating Helicobacter pylori from the stomach mucosa of the patient with gastritis and p...

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Autores principales:	O. K. Pozdeev, A. O. Pozdeeva, Yu. V. Valeeva, P. E. Gulyaev, A. N. Savinova
Formato:	article
Lenguaje:	RU
Publicado:	Sankt-Peterburg : NIIÈM imeni Pastera 2019
Materias:	helicobacter pylori cytokines gastric mucosal epitheliocytes Infectious and parasitic diseases RC109-216
Acceso en línea:	https://doaj.org/article/01dd16f030f1470f9f9e894fa591de57
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spelling	oai:doaj.org-article:01dd16f030f1470f9f9e894fa591de572021-11-22T07:09:52ZMechanisms of interacting <i>Helicobacter pylori</i> with gastric mucosal epithelium. II. A reaction of gastric epithelium on <i>Helicobacter pylori</i> colonization and persistence2220-76192313-739810.15789/2220-7619-2019-2-253-261https://doaj.org/article/01dd16f030f1470f9f9e894fa591de572019-07-01T00:00:00Zhttps://www.iimmun.ru/iimm/article/view/635https://doaj.org/toc/2220-7619https://doaj.org/toc/2313-7398Gastric and duodenal recurrent inflammatory diseases have a high prevalence, but the role played by microbes in its development remained unclear. However, the data published in 1983 by Marshall and Warren about isolating Helicobacter pylori from the stomach mucosa of the patient with gastritis and proposing relevant cultivation methods was the turning point in investigating etiology of the upper digestive tract inflammatory disorders. Moreover, it was shown that the majority of H. pylori spp. are found within the gastric lumen upon colonization, whereas around 20% of them are attached to the epithelial cells in the stomach. In addition, effects of interacting H. pylori with gastric epithelium and activation of some defense mechanisms due to bacterial colonization and spreading were analyzed. It was found that along with triggering pro-inflammatory response induced by proteins VacA as well as phosphorylated/unphosphorylated CagA, wherein the latter is able to induce a set of protective reactions H. pylori disrupts intercellular contacts, affects epithelial cell polarity and proliferation, and activates SHP-2 phosphatase resulting in emerging diverse types of cellular responses. The activation mechanisms for the mitogen-activated protein kinase (MAPK) pathway were discussed. The ability of H. pylori to regulate apoptosis, particularly via its suppression, by expressing ERK kinase and protein MCL1 facilitating bacterial survival in the gastric mucosa as well as beneficial effects related to bacterial circulation on gastric epithelial cell survival elicited by anti-apoptotic factors were also examined. Of note, persistence of H. pylori are mainly determined by activating transcriptional factors including NF-κB, NFAT, SRF, T-cell lymphoid enhancing factor (TCF/LEF), regulating activity of MCL1 protein, in turn, being one of the main anti-apoptotic factors, as well as induced production of the migration inhibitory factor (MIF). The role of VacA cytotoxin in triggering epithelial cell apoptosis via caspase-mediated pathways was also considered. Infection with H. pylori is accompanied by release of proinflammatory cytokine cocktail detected both in vitro and in vivo. In particular, bacterial urease activating transcriptional factor NF-κB was shown to play a crucial role in inducing cytokine production. Moreover, such signaling pathways may be activated after H. pylori is attached to the cognate receptor in the gastric epithelial surface by interacting with CD74 and MHC class II molecules. Finally, a role for various CD4+ T cell subsets, particularly type 17 T helper cells (Th17) in inducing immune response against H. pylori antigens in gastric mucosa was revealed were also discussed.O. K. PozdeevA. O. PozdeevaYu. V. ValeevaP. E. GulyaevA. N. SavinovaSankt-Peterburg : NIIÈM imeni Pasteraarticlehelicobacter pyloricytokinesgastric mucosal epitheliocytesInfectious and parasitic diseasesRC109-216RUInfekciâ i Immunitet, Vol 9, Iss 2, Pp 253-261 (2019)
institution	DOAJ
collection	DOAJ
language	RU
topic	helicobacter pylori cytokines gastric mucosal epitheliocytes Infectious and parasitic diseases RC109-216
spellingShingle	helicobacter pylori cytokines gastric mucosal epitheliocytes Infectious and parasitic diseases RC109-216 O. K. Pozdeev A. O. Pozdeeva Yu. V. Valeeva P. E. Gulyaev A. N. Savinova Mechanisms of interacting <i>Helicobacter pylori</i> with gastric mucosal epithelium. II. A reaction of gastric epithelium on <i>Helicobacter pylori</i> colonization and persistence
description	Gastric and duodenal recurrent inflammatory diseases have a high prevalence, but the role played by microbes in its development remained unclear. However, the data published in 1983 by Marshall and Warren about isolating Helicobacter pylori from the stomach mucosa of the patient with gastritis and proposing relevant cultivation methods was the turning point in investigating etiology of the upper digestive tract inflammatory disorders. Moreover, it was shown that the majority of H. pylori spp. are found within the gastric lumen upon colonization, whereas around 20% of them are attached to the epithelial cells in the stomach. In addition, effects of interacting H. pylori with gastric epithelium and activation of some defense mechanisms due to bacterial colonization and spreading were analyzed. It was found that along with triggering pro-inflammatory response induced by proteins VacA as well as phosphorylated/unphosphorylated CagA, wherein the latter is able to induce a set of protective reactions H. pylori disrupts intercellular contacts, affects epithelial cell polarity and proliferation, and activates SHP-2 phosphatase resulting in emerging diverse types of cellular responses. The activation mechanisms for the mitogen-activated protein kinase (MAPK) pathway were discussed. The ability of H. pylori to regulate apoptosis, particularly via its suppression, by expressing ERK kinase and protein MCL1 facilitating bacterial survival in the gastric mucosa as well as beneficial effects related to bacterial circulation on gastric epithelial cell survival elicited by anti-apoptotic factors were also examined. Of note, persistence of H. pylori are mainly determined by activating transcriptional factors including NF-κB, NFAT, SRF, T-cell lymphoid enhancing factor (TCF/LEF), regulating activity of MCL1 protein, in turn, being one of the main anti-apoptotic factors, as well as induced production of the migration inhibitory factor (MIF). The role of VacA cytotoxin in triggering epithelial cell apoptosis via caspase-mediated pathways was also considered. Infection with H. pylori is accompanied by release of proinflammatory cytokine cocktail detected both in vitro and in vivo. In particular, bacterial urease activating transcriptional factor NF-κB was shown to play a crucial role in inducing cytokine production. Moreover, such signaling pathways may be activated after H. pylori is attached to the cognate receptor in the gastric epithelial surface by interacting with CD74 and MHC class II molecules. Finally, a role for various CD4+ T cell subsets, particularly type 17 T helper cells (Th17) in inducing immune response against H. pylori antigens in gastric mucosa was revealed were also discussed.
format	article
author	O. K. Pozdeev A. O. Pozdeeva Yu. V. Valeeva P. E. Gulyaev A. N. Savinova
author_facet	O. K. Pozdeev A. O. Pozdeeva Yu. V. Valeeva P. E. Gulyaev A. N. Savinova
author_sort	O. K. Pozdeev
title	Mechanisms of interacting <i>Helicobacter pylori</i> with gastric mucosal epithelium. II. A reaction of gastric epithelium on <i>Helicobacter pylori</i> colonization and persistence
title_short	Mechanisms of interacting <i>Helicobacter pylori</i> with gastric mucosal epithelium. II. A reaction of gastric epithelium on <i>Helicobacter pylori</i> colonization and persistence
title_full	Mechanisms of interacting <i>Helicobacter pylori</i> with gastric mucosal epithelium. II. A reaction of gastric epithelium on <i>Helicobacter pylori</i> colonization and persistence
title_fullStr	Mechanisms of interacting <i>Helicobacter pylori</i> with gastric mucosal epithelium. II. A reaction of gastric epithelium on <i>Helicobacter pylori</i> colonization and persistence
title_full_unstemmed	Mechanisms of interacting <i>Helicobacter pylori</i> with gastric mucosal epithelium. II. A reaction of gastric epithelium on <i>Helicobacter pylori</i> colonization and persistence
title_sort	mechanisms of interacting <i>helicobacter pylori</i> with gastric mucosal epithelium. ii. a reaction of gastric epithelium on <i>helicobacter pylori</i> colonization and persistence
publisher	Sankt-Peterburg : NIIÈM imeni Pastera
publishDate	2019
url	https://doaj.org/article/01dd16f030f1470f9f9e894fa591de57
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Mechanisms of interacting <i>Helicobacter pylori</i> with gastric mucosal epithelium. II. A reaction of gastric epithelium on <i>Helicobacter pylori</i> colonization and persistence

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