<abstract xmlns="http://www.w3.org/1999/xhtml"><italic>Helicobacter pylori</italic> commonly colonizes the human gastric mucosa. Infections with this microorganism can contribute to serious health consequences, such as peptic ulceration, gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue lymphoma. Chronic persistence of this bacteria in the host organism is probably strongly dependent on the secretion of outer membrane vesicles (OMV). These organelles are small, electron-dense, extracellular structures which are secreted in large amounts during stressful conditions, among others. <italic>H. pylori</italic> OMV mediate transfer of virulence factors such as toxins and immunomodulatory compounds. They contribute to avoiding a response from the host immune system and inducing chronic gastritis. OMV secretion also affects the formation of cell aggregates, microcolonies and biofilm matrix. Enhanced OMV production is connected to maintenance of direct contact through cell-cell and cell-surface interactions. A key component of OMV, which determines their structural function, is extracellular DNA (eDNA) anchored to the surface of these organelles. eDNA associated with OMV additionally determines the genetic recombination in the process of horizontal gene transfer. <italic>H. pylori</italic> is naturally competent for genetic transformation and is constantly capable of DNA uptake from the environment. The natural competence state promotes the assimilation of eDNA anchored to the OMV surface. This is probably dependent on ComB and ComEC components, which are involved in the transformation process. For this reason, the OMV secretion mediates intensive exchange of genetic material, promotes adaptation to changing environmental conditions and enables persistent infecting of the gastric mucosa by <italic>H. pylori</italic>.1. Introduction. 2. Secretion of outer membrane vesicles by <italic>H. pylori.</italic> 3. Proteome of <italic>H. pylori</italic> outer membrane vesicles. 4. Transport of virulence factors through OMV. 4.1. Toxin VacA. 4.2. Oncoprotein CagA. 4.3. Other substances. 5. OMV involvement in biofilm formation. 5.1. Functions of biofilm. 5.2. OMV influence on bacterial biofilm formation. 5.3. OMV influence on biofilm formation by <italic>H. pylori.</italic> 5.4. Structural function of <italic>H. pylori</italic> extracellular DNA. 6. Extracellular DNA as an information carrier. 6.1. Influence on virulence. 6.2. Transformation. 6.3. Natural competence of <italic>H. pylori</italic>. 7. Conclusions</abstract>

Helicobacter pylori commonly colonizes the human gastric mucosa. Infections with this microorganism can contribute to serious health consequences, such as peptic ulceration, gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue lymphoma. Chronic persistence of this bacteria in the host organism is probably strongly dependent on the secretion of outer membrane vesicles (OMV). These organelles are small, electron-dense, extracellular structures which are secreted in large amounts during stressful conditions, among others. H. pylori OMV mediate transfer of virulence factors such as toxins and immunomodulatory compounds. They contribute to avoiding a response from the host immune system and inducing chronic gastritis. OMV secretion also affects the formation of cell aggregates, microcolonies and biofilm matrix. Enhanced OMV production is connected to maintenance of direct contact through cell-cell and cell-surface interactions. A key component of OMV, which determines their structural function, is extracellular DNA (eDNA) anchored to the surface of these organelles. eDNA associated with OMV additionally determines the genetic recombination in the process of horizontal gene transfer. H. pylori is naturally competent for genetic transformation and is constantly capable of DNA uptake from the environment. The natural competence state promotes the assimilation of eDNA anchored to the OMV surface. This is probably dependent on ComB and ComEC components, which are involved in the transformation process. For this reason, the OMV secretion mediates intensive exchange of genetic material, promotes adaptation to changing environmental conditions and enables persistent infecting of the gastric mucosa by H. pylori.1. Introduction. 2. Secretion of outer membrane vesicles by H. pylori. 3. Proteome of H. pylori outer membrane vesicles. 4. Transport of virulence factors through OMV. 4.1. Toxin VacA. 4.2. Oncoprotein CagA. 4.3. Other substances. 5. OMV involvement in biofilm formation. 5.1. Functions of biofilm. 5.2. OMV influence on bacterial biofilm formation. 5.3. OMV influence on biofilm formation by H. pylori. 5.4. Structural function of H. pylori extracellular DNA. 6. Extracellular DNA as an information carrier. 6.1. Influence on virulence. 6.2. Transformation. 6.3. Natural competence of H. pylori. 7. Conclusions

Secretion of outer membrane vesicles as a mechanism promoting <italic>H. pylori</italic> infections

Advancements of Microbiology

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Secretion of outer membrane vesicles as a mechanism promoting  infections

<trans-abstract xml:lang="pl" xmlns="http://www.w3.org/1999/xhtml">1. Wstęp. 2. Sekrecja pęcherzyków błonowych u <italic>H. pylori.</italic> 3. Proteom pęcherzyków błonowych <italic>H. pylori</italic>. 4. Transport czynników wirulencji poprzez OMV. 4.1. Toksyna VacA. 4.2. Onkoproteina CagA. 4.3. Inne substancje. 5. Udział OMV w formowaniu biofilmu. 5.1. Funkcje biofilmu. 5.2. Zaangażowanie OMV w tworzenie biofilmu u bakterii. 5.3. Zaangażowanie OMV w tworzenie biofilmu u <italic>H. pylori.</italic>5.4. Funkcja strukturalna zewnątrzkomórkowego DNA <italic>H. pylori.</italic> 6. Zewnątrzkomórkowe DNA jako nośnik informacji. 6.1. Wpływ na wirulencję. 6.2. Transformacja. 6.3. Naturalna kompetencja <italic>H. pylori.</italic> 7. Podsumowanie</trans-abstract>

1. Wstęp. 2. Sekrecja pęcherzyków błonowych u H. pylori. 3. Proteom pęcherzyków błonowych H. pylori. 4. Transport czynników wirulencji poprzez OMV. 4.1. Toksyna VacA. 4.2. Onkoproteina CagA. 4.3. Inne substancje. 5. Udział OMV w formowaniu biofilmu. 5.1. Funkcje biofilmu. 5.2. Zaangażowanie OMV w tworzenie biofilmu u bakterii. 5.3. Zaangażowanie OMV w tworzenie biofilmu u H. pylori.5.4. Funkcja strukturalna zewnątrzkomórkowego DNA H. pylori. 6. Zewnątrzkomórkowe DNA jako nośnik informacji. 6.1. Wpływ na wirulencję. 6.2. Transformacja. 6.3. Naturalna kompetencja H. pylori. 7. Podsumowanie

SEKRECJA PĘCHERZYKÓW BŁONOWYCH JAKO MECHANIZM PROMUJĄCY INFEKCJE

Helicobacter pylori commonly colonizes the human gastric mucosa. Infections with this microorganism can contribute to serious health consequences, such as...

Secretion of outer membrane vesicles as a mechanism promoting H. pylori infections

Online veröffentlicht: 22. Mai 2019

Seitenbereich: 316 - 325

Eingereicht: 01. Jan. 2017

Akzeptiert: 01. März 2017

DOI: https://doi.org/10.21307/PM-2017.56.3.316

2017 @ Author., Published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.