The Human Stomach in Health and Disease: Infection Strategies by Helicobacter pylori

Robinson, Karen; Letley, Darren P.; Kaneko, Kazuyo

doi:10.1007/978-3-319-50520-6_1

Cited by 20 publications

(18 citation statements)

References 127 publications

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“…Helicobacter pylori is a Gram-negative, microaerophilic bacterium that inhabits the stomach mucosa [ 1 – 3 ]. Colonisation with this pathogen is often associated with the development of numerous digestive system disorders, i.e.…”

Section: Introductionmentioning

confidence: 99%

“…gastritis, peptic ulcer disease (10–15%), gastric cancer (1–3%), and mucosa associated lymphoid tissue (MALT) lymphoma (< 0.1%) [ 4 ]. The type and severity of diseases depend on many factors, among them: the status of the host’s immune system, the pathogenicity of H. pylori strains, and the presence of environmental factors (diet, stress, hygiene level, or the presence of co-infections) [ 1 ]. Within these, the most attention is paid to the pathogenicity of H. pylori and the variety of virulence factors produced by these bacteria.…”

Section: Introductionmentioning

confidence: 99%

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Morphology of Helicobacter pylori as a result of peptidoglycan and cytoskeleton rearrangements

Krzyżek¹,

Gościniak²

2018

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Helicobacter pylori is a Gram-negative, microaerophilic bacterium colonising the gastric mucosa. Normally, this bacterium has a spiral shape, which is crucial for proper colonisation of the stomach and cork-screwing penetration of dense mucin covering this organ. However, H. pylori may also form curved/straight rods, filamentous forms and coccoid forms. This morphological variability affects nutrient transport and respiration processes, as well as motility, the ability to form aggregates/biofilms, and resistance to adverse environmental factors. For this reason, a more accurate understanding of the molecular determinants that control the morphology of H. pylori seems to be crucial in increasing the effectiveness of antibacterial therapies directed against this microorganism. This article focuses on the molecular factors responsible for peptidoglycan and cytoskeleton rearrangements affecting H. pylori morphology and survivability. In addition, the existence of proteins associated with modifications of H. pylori morphology as potential targets in therapies reducing the virulence of this bacterium has been suggested.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Morphology of Helicobacter pylori as a result of peptidoglycan and cytoskeleton rearrangements

Krzyżek¹,

Gościniak²

2018

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“…Helicobacter pylori is a Gram-negative, flagellated pathogen, which persistently colonizes the human stomach [1, 2]. About 50% of the world population carries these bacteria, and infections are associated with chronic, often asymptomatic gastritis in all infected individuals.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of serine protease HtrA enhances disruption of adherens junctions, paracellular transmigration and type IV secretion of CagA by Helicobacter pylori

et al. 2017

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BackgroundThe serine protease HtrA is an important factor for regulating stress responses and protein quality control in bacteria. In recent studies, we have demonstrated that the gastric pathogen Helicobacter pylori can secrete HtrA into the extracellular environment, where it cleaves-off the ectodomain of the tumor suppressor and adherens junction protein E-cadherin on gastric epithelial cells.ResultsE-cadherin cleavage opens cell-to-cell junctions, allowing paracellular transmigration of the bacteria across polarized monolayers of MKN-28 and Caco-2 epithelial cells. However, rapid research progress on HtrA function is mainly hampered by the lack of ΔhtrA knockout mutants, suggesting that htrA may represent an essential gene in H. pylori. To circumvent this major handicap and to investigate the role of HtrA further, we overexpressed HtrA by introducing a second functional htrA gene copy in the chromosome and studied various virulence properties of the bacteria. The resulting data demonstrate that overexpression of HtrA in H. pylori gives rise to elevated rates of HtrA secretion, cleavage of E-cadherin, bacterial transmigration and delivery of the type IV secretion system (T4SS) effector protein CagA into polarized epithelial cells, but did not affect IL-8 chemokine production or the secretion of vacuolating cytotoxin VacA and γ-glutamyl-transpeptidase GGT.ConclusionsThese data provide for the first time genetic evidence in H. pylori that HtrA is a novel major virulence factor controlling multiple pathogenic activities of this important microbe.

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“…Successful gastric colonization by any microorganism in this microniche is due to the existence of various abilities to avoid hostile acidic conditions and the viscous mucosal layer[17,18]. To do this, H. pylori harbors specific features leading to successful colonization.…”

Section: First Strategy: Escaping Gastric Aciditymentioning

confidence: 99%

“…The acidity of the stomach (pH 1-2) is the first danger to threaten bacterial survival in the stomach[14,17,19]. H. pylori is able to survive at approximately pH 5 which can kill many digested organisms within a few minutes after acid exposure.…”

Section: Urease As the First Weapon Against Aciditymentioning

confidence: 99%

Strategies used byhelicobacter pylorito establish persistent infection

Abadi

2017

WJG

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Helicobacter pylori (H. pylori) is a Gram-negative and motile bacterium that colonizes the hostile microniche of the human stomach, then persists for the host’s entire life, if not effectively treated. Clinically, H. pylori plays a causative role in the development of a wide spectrum of diseases including chronic active gastritis, peptic ulceration, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue lymphoma. Due to the global distribution of H. pylori, it is no exaggeration to conclude that smart strategies are contributing to adaptation of the bacterium to its permanent host. Thirty-four years after the discovery of this bacterium, there are still many unanswered questions. For example, which strategies help the bacterium to survive in this inhospitable microniche? This question is slightly easier to answer if we presume the same clinical concept for both persistent infection and disease. Understanding the mechanisms governing H. pylori persistence will improve identification of the increased risk of diseases such as gastric cancer in patients infected with this bacterium. A well-defined and long-term equilibrium between the human host and H. pylori allows bacterial persistence in the gastric microniche; although this coexistence leads to a high risk of severe diseases such as gastric cancer. To escape the bactericidal activity of stomach acid, H. pylori secretes large amounts of surface-associated and cytosolic urease. The potential to avoid acidic conditions and immune evasion are discussed in order to explain the persistence of H. pylori colonization in the gastric mucosa, and data on bacterial genetic diversity are included. Information on the mechanisms related to H. pylori persistence can also provide the direction for future research concerning effective therapy and management of gastroduodenal disorders. The topics presented in the current review are important for elucidating the strategies used by H. pylori to help the bacterium persist in relation to the immune system and the many unfavorable features of living in the gastric microniche.

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The Human Stomach in Health and Disease: Infection Strategies by Helicobacter pylori

Cited by 20 publications

References 127 publications

Morphology of Helicobacter pylori as a result of peptidoglycan and cytoskeleton rearrangements

Morphology of Helicobacter pylori as a result of peptidoglycan and cytoskeleton rearrangements

Overexpression of serine protease HtrA enhances disruption of adherens junctions, paracellular transmigration and type IV secretion of CagA by Helicobacter pylori

Strategies used byhelicobacter pylorito establish persistent infection

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