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Helicobacter pylori Extracellular Proteins and Cell Surface Structures: Towards Novel Therapeutics

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Microbiology".

Deadline for manuscript submissions: 20 November 2024 | Viewed by 2344

Special Issue Editor


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Guest Editor
1. Infection and Immunity Program, Monash Biomedicine Discovery Institute, Department of Microbiology, Monash University, Clayton, VIC 3800, Australia
2. Infection and Immunity Program, Monash Biomedicine Discovery Institute, Department of Biochemistry and Molecular Biology, Monash University, Clayton, VIC 3800, Australia
Interests: Helicobacter pylori; infection and immunity; gastric cancer

Special Issue Information

Dear Colleagues,

Helicobacter pylori maintains a cancer-promoting chronic infection of the human stomach via perfect adaptation to the harsh gastric environment, and by evading all host immune defences. While secreted soluble H. pylori proteins and structures coating the H. pylori cell surface play critical roles in both of these mechanisms of persistence, the biological functions of many of these factors remain to be elucidated. This is particularly so for the numerous secreted soluble proteins and outer membrane protein adhesins unique to H. pylori. In light of increasing antimicrobial resistance, interception of these extracellular proteins or structures could hold the key to treating or preventing H. pylori infection and life-threatening associated gastric diseases.

This Special Issue focuses on the extracellular proteins and surface structures of H. pylori in relation to infection and disease. We welcome original research papers, comprehensive reviews and novel communications dealing with structure-function of H. pylori cell surface-bound or secreted soluble molecules, their diversity, their roles in host–pathogen interactions and immune evasion, and their potential for targeting in therapeutic and prophylactic strategies.

Dr. Terry Kwok
Guest Editor

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Keywords

  • Helicobacter pylori
  • outer membrane protein
  • lipopolysaccharide
  • secreted soluble proteins
  • protease
  • antigenic diversity
  • adhesin
  • phase variation
  • gastric cancer

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Published Papers (1 paper)

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Research

12 pages, 4018 KiB  
Communication
HtrA-Dependent E-Cadherin Shedding Impairs the Epithelial Barrier Function in Primary Gastric Epithelial Cells and Gastric Organoids
by Marina Canadas-Ortega, Iris Mühlbacher, Gernot Posselt, Sebastian Diechler, Christian Daniel Ferner, Francesco Boccellato, Oliver Owen Koch, Daniel Neureiter, Michael Weitzendorfer, Klaus Emmanuel and Silja Wessler
Int. J. Mol. Sci. 2024, 25(13), 7083; https://doi.org/10.3390/ijms25137083 - 27 Jun 2024
Viewed by 1933
Abstract
Impaired E-cadherin (Cdh1) functions are closely associated with cellular dedifferentiation, infiltrative tumor growth and metastasis, particularly in gastric cancer. The class-I carcinogen Helicobacter pylori (H. pylori) colonizes gastric epithelial cells and induces Cdh1 shedding, which is primarily mediated by the secreted [...] Read more.
Impaired E-cadherin (Cdh1) functions are closely associated with cellular dedifferentiation, infiltrative tumor growth and metastasis, particularly in gastric cancer. The class-I carcinogen Helicobacter pylori (H. pylori) colonizes gastric epithelial cells and induces Cdh1 shedding, which is primarily mediated by the secreted bacterial protease high temperature requirement A (HtrA). In this study, we used human primary epithelial cell lines derived from gastroids and mucosoids from different healthy donors to investigate HtrA-mediated Cdh1 cleavage and the subsequent impact on bacterial pathogenesis in a non-neoplastic context. We found a severe impairment of Cdh1 functions by HtrA-induced ectodomain cleavage in 2D primary cells and mucosoids. Since mucosoids exhibit an intact apico-basal polarity, we investigated bacterial transmigration across the monolayer, which was partially depolarized by HtrA, as indicated by microscopy, the analyses of the transepithelial electrical resistance (TEER) and colony forming unit (cfu) assays. Finally, we investigated CagA injection and observed efficient CagA translocation and tyrosine phosphorylation in 2D primary cells and, to a lesser extent, similar effects in mucosoids. In summary, HtrA is a crucially important factor promoting the multistep pathogenesis of H. pylori in non-transformed primary gastric epithelial cells and organoid-based epithelial models. Full article
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