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Pathogenicity and Antibiotic Resistance of Helicobacter pylori

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: 30 July 2025 | Viewed by 2864

Special Issue Editor


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Guest Editor
Department of Medical Microbiology, Wroclaw Medical University, 50-368 Wroclaw, Poland
Interests: Helicobacter pylori; biofilm; coccoid forms; morphology; outer membrane vesicles; antibiotic tolerance; antimicrobial/antibiofilm activity
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Special Issue Information

Dear Colleagues,

Helicobacter pylori is one of the most common human pathogens. Even though more than 40 years have passed since its discovery, knowledge about methods aimed at effective control of this bacterium is still insufficient. The reason for this impasse is strictly linked to a wide range of virulence factors enabling this pathogen for the establishment of a chronic infection and its easiness of acquiring mechanisms of antibiotic resistance/tolerance.

Therefore, the main goal of this Special Issue is to encourage scientists and clinicians to share the latest scientific reports on the pathogenicity and antibiotic resistance of Helicobacter pylori. As part of the Special Issue, authors are encouraged to submit original research papers, short communications and reviews describing the molecular phenomena responsible for the pathogenesis of this bacterium (adhesins, toxins, enzymes), as well as the development of both antibiotic resistance (point mutations) and antibiotic tolerance (efflux pumps, biofilm formation, transition into coccoid forms and secretion of membrane vesicles).

Dr. Paweł Krzyżek
Guest Editor

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Keywords

  • Helicobacter pylori
  • antibiotic resistance
  • antibiotic tolerance
  • point mutations
  • efflux pumps
  • biofilm formation
  • coccoid forms
  • membrane vesicles
  • virulence factors

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Published Papers (2 papers)

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Research

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18 pages, 18776 KiB  
Article
Optimization of Helicobacter pylori Biofilm Formation in In Vitro Conditions Mimicking Stomach
by Paweł Krzyżek, Paweł Migdał, Barbara Krzyżanowska and Anna Duda-Madej
Int. J. Mol. Sci. 2024, 25(18), 9839; https://doi.org/10.3390/ijms25189839 - 11 Sep 2024
Viewed by 1550
Abstract
Helicobacter pylori is one of the most common bacterial pathogens worldwide and the main etiological agent of numerous gastric diseases. The frequency of multidrug resistance of H. pylori is growing and the leading factor related to this phenomenon is its ability to form [...] Read more.
Helicobacter pylori is one of the most common bacterial pathogens worldwide and the main etiological agent of numerous gastric diseases. The frequency of multidrug resistance of H. pylori is growing and the leading factor related to this phenomenon is its ability to form biofilm. Therefore, the establishment of a proper model to study this structure is of critical need. In response to this, the aim of this original article is to validate conditions of the optimal biofilm development of H. pylori in monoculture and co-culture with a gastric cell line in media simulating human fluids. Using a set of culture-based and microscopic techniques, we proved that simulated transcellular fluid and simulated gastric fluid, when applied in appropriate concentrations, stimulate autoaggregation and biofilm formation of H. pylori. Additionally, using a co-culture system on semi-permeable membranes in media imitating the stomach environment, we were able to obtain a monolayer of a gastric cell line with H. pylori biofilm on its surface. We believe that the current model for H. pylori biofilm formation in monoculture and co-culture with gastric cells in media containing host-mimicking fluids will constitute a platform for the intensification of research on H. pylori biofilms in in vitro conditions that simulate the human body. Full article
(This article belongs to the Special Issue Pathogenicity and Antibiotic Resistance of Helicobacter pylori)
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Review

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16 pages, 512 KiB  
Review
The Role of Helicobacter pylori Heat Shock Proteins in Gastric Diseases’ Pathogenesis
by Olga Maria Manna, Celeste Caruso Bavisotto, Melania Ionelia Gratie, Provvidenza Damiani, Giovanni Tomasello and Francesco Cappello
Int. J. Mol. Sci. 2025, 26(11), 5065; https://doi.org/10.3390/ijms26115065 - 24 May 2025
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Abstract
Helicobacter pylori (H. pylori) is a Gram-negative bacterium that colonizes the human stomach and is associated with several gastric diseases, including gastritis, peptic ulcer disease, and gastric cancer. The bacterium’s ability to thrive in the harsh gastric environment is due, to [...] Read more.
Helicobacter pylori (H. pylori) is a Gram-negative bacterium that colonizes the human stomach and is associated with several gastric diseases, including gastritis, peptic ulcer disease, and gastric cancer. The bacterium’s ability to thrive in the harsh gastric environment is due, to some extent, to its stress response mechanisms, with its heat shock proteins (HSPs) playing a putative, yet not fully understood, role in these adaptive processes. HSPs are a family of molecules, highly conserved throughout phylogenesis, that assist in protein folding, prevent aggregation, and ensure cellular homeostasis under stressful conditions. In H. pylori, HSPs contribute to survival in the stomach’s acidic environment and oxidative stress. Furthermore, they aid in the bacterium’s ability to adhere to gastric epithelial cells, modulate the host immune response, and form biofilms, all contributing to chronic infection and pathogenicity. The role of microbial HSPs in antibiotic resistance has also emerged as a critical area of research, as these proteins help stabilize efflux pumps, protect essential proteins targeted by antibiotics, and promote biofilm formation, thereby reducing the efficacy of antimicrobial treatments. Among bacterial HSPs, GroEL and DnaK are probably the major proteins that control most of the H. pylori’s functioning. Indeed, both proteins possess remarkable acid resistance, high substrate affinity, and dual roles in protein homeostasis and host interaction. These features make them critical for H. pylori’s adaptation, persistence, and pathogenicity in the gastric niche. In addition, recent findings have also highlighted the involvement of HSPs in the crosstalk between H. pylori and gastric epithelial cells mediated by the release of bacterial outer membrane vesicles and host-derived exosomes, both of these extracellular vesicles being part of the muco-microbiotic layer of the stomach and influencing cellular signalling and immune modulation. Considering their critical role in the survival and persistence of bacteria, microbial HSPs also represent potential therapeutic targets. Strategies aimed at inhibiting microbial HSP function, combined with conventional antibiotics or developing vaccines targeting microbial HSPs, could provide new avenues for the treatment of H. pylori infections and combat antibiotic resistance. This review explores the multifaceted roles of microbial HSPs in the pathogenesis of H. pylori, highlighting their contributions to bacterial adhesion, immune evasion, stress response, and antibiotic resistance. Full article
(This article belongs to the Special Issue Pathogenicity and Antibiotic Resistance of Helicobacter pylori)
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