Special Issue "Helicobacter pylori Infection–Inducement of Gastroenteric Diseases"

A special issue of Toxins (ISSN 2072-6651). This special issue belongs to the section "Bacterial Toxins".

Deadline for manuscript submissions: closed (31 August 2019).

Special Issue Editor

Prof. Dr. Vittorio Ricci
E-Mail Website
Guest Editor
Department of Molecular Medicine, Human Physiology Unit, University of Pavia Medical School,Via Forlanini 6, 27100 Pavia, Italy
Interests: bacterial protein toxins; host-pathogen interactions in gastrointestinal tract; helicobacter pylori; infection and gastrointestinal cancer

Special Issue Information

Dear Colleagues,

For almost a century, gastric acid has been considered the most significant offensive factor for the human stomach, a sort of an “enemy inside”. Karl Schwarz’s aphorism of 1910, “no acid, no ulcer”, became a paradigm that paved the way to all the therapeutic approaches to gastritis and peptic ulcers until the early 1980s, when people were obliged to discard all the existing gastroenterology textbooks. This was because Helicobacter pylori was discovered and its pivotal relevance in the most severe gastric diseases rapidly demonstrated: a true revolution in the field.

H. pylori colonizes the stomach of about half the global population, making it one of the most common bacterial infections worldwide. If untreated, the infection becomes chronic and persists throughout life despite a vigorous immune response. H. pylori infection always causes active chronic gastritis that can remain clinically silent for many years after initial infection, due to the dynamic equilibrium between the bacterium and its human host. H. pylori infection may however evolve into more severe diseases, such as atrophic gastritis, peptic ulcer, mucosa-associated lymphoid tissue (MALT) lymphoma, or gastric adenocarcinoma. H. pylori infection is the strongest known risk factor for gastric malignancy and its relevance for gastric cancer development is quite similar to that of tobacco smoking for lung cancer.

H. pylori-induced pathology is the result of a well-choreographed interaction between the pathogen and its host, which is in turn dependent on specific bacterial virulence factors/products (e.g., VacA vacuolating toxin, CagA, HtrA, γ-glutamyl transpeptidase), host genotypic traits and permissive environmental factors.

This Special Issue is aimed at gathering the most recent cutting-edge research on H. pylori strategies and tools to circumvent the defensive capabilities of the host, subverting normal cell function in directions favourable for the bacterium even though, unfortunately, it has a high pathogenic potential for the human host. Both reviews and original papers from clinical and experimental scientists are welcome.

Prof. Vittorio Ricci
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a double-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2400 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Helicobacter pylori
  • host–pathogen interactions
  • virulence factors
  • pathogenic mechanisms
  • cell internalization and intracellular trafficking
  • signal transduction
  • gastric epithelial barrier
  • gastritis and peptic ulcer
  • gastric cancer
  • mucosal immunology

Published Papers (3 papers)

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Research

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Article
CagA Effector Protein in Helicobacter pylori-Infected Human Gastric Epithelium in Vivo: From Bacterial Core and Adhesion/Injection Clusters to Host Cell Proteasome-Rich Cytosol
Toxins 2019, 11(11), 618; https://doi.org/10.3390/toxins11110618 - 25 Oct 2019
Cited by 1 | Viewed by 1040
Abstract
A key role in the carcinogenic action of Helicobacter pylori is played by the effector protein CagA, the first identified oncoprotein of the bacterial world. However, the present knowledge in regard to the bacterial injection of CagA into epithelial cells (through a type [...] Read more.
A key role in the carcinogenic action of Helicobacter pylori is played by the effector protein CagA, the first identified oncoprotein of the bacterial world. However, the present knowledge in regard to the bacterial injection of CagA into epithelial cells (through a type IV secretion system) and its intracellular fate is based primarily on experimental studies in vitro. Our study was aimed to investigate, in H. pylori-infected human gastric epithelium, CagA delivery and intracellular distribution in order to identify any in vivo counterpart of the cell injection mechanism described in vitro and any intracellular cytoplasmic site of preferential CagA distribution, thus shedding light on the natural history of CagA in vivo. By transmission electron microscopy and ultrastructural immunocytochemistry (which combine precise molecule localization with detailed analysis of bacterial-host cell interaction and epithelial cell ultrastructure), we investigated endoscopic biopsies of gastric antrum from H. pylori-infected dyspeptic patients. Our findings provide support for CagA direct injection into gastric epithelial cells at bacterial adhesion sites located on the lateral plasma membrane and for its cytosolic intracellular distribution with selective concentration inside peculiar proteasome-rich areas, which might be site not only of CagA degradation but also of CagA-promoted crucial events in gastric carcinogenesis. Full article
(This article belongs to the Special Issue Helicobacter pylori Infection–Inducement of Gastroenteric Diseases)
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Review

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Review
Helicobacter pylori Virulence Factors Exploiting Gastric Colonization and its Pathogenicity
Toxins 2019, 11(11), 677; https://doi.org/10.3390/toxins11110677 - 19 Nov 2019
Cited by 34 | Viewed by 2677
Abstract
Helicobacter pylori colonizes the gastric epithelial cells of at least half of the world’s population, and it is the strongest risk factor for developing gastric complications like chronic gastritis, ulcer diseases, and gastric cancer. To successfully colonize and establish a persistent infection, the [...] Read more.
Helicobacter pylori colonizes the gastric epithelial cells of at least half of the world’s population, and it is the strongest risk factor for developing gastric complications like chronic gastritis, ulcer diseases, and gastric cancer. To successfully colonize and establish a persistent infection, the bacteria must overcome harsh gastric conditions. H. pylori has a well-developed mechanism by which it can survive in a very acidic niche. Despite bacterial factors, gastric environmental factors and host genetic constituents together play a co-operative role for gastric pathogenicity. The virulence factors include bacterial colonization factors BabA, SabA, OipA, and HopQ, and the virulence factors necessary for gastric pathogenicity include the effector proteins like CagA, VacA, HtrA, and the outer membrane vesicles. Bacterial factors are considered more important. Here, we summarize the recent information to better understand several bacterial virulence factors and their role in the pathogenic mechanism. Full article
(This article belongs to the Special Issue Helicobacter pylori Infection–Inducement of Gastroenteric Diseases)
Review
Tyrosine Kinases in Helicobacter pylori Infections and Gastric Cancer
Toxins 2019, 11(10), 591; https://doi.org/10.3390/toxins11100591 - 11 Oct 2019
Cited by 3 | Viewed by 1500
Abstract
Helicobacter pylori (H. pylori) has been identified as a leading cause of gastric cancer, which is one of the most frequent and malignant types of tumor. It is characterized by its rapid progression, distant metastases, and resistance to conventional chemotherapy. A [...] Read more.
Helicobacter pylori (H. pylori) has been identified as a leading cause of gastric cancer, which is one of the most frequent and malignant types of tumor. It is characterized by its rapid progression, distant metastases, and resistance to conventional chemotherapy. A number of receptor tyrosine kinases and non-receptor tyrosine kinases have been implicated in H. pylori-mediated pathogenesis and tumorigenesis. In this review, recent findings of deregulated EGFR, c-Met, JAK, FAK, Src, and c-Abl and their functions in H. pylori pathogenesis are summarized. Full article
(This article belongs to the Special Issue Helicobacter pylori Infection–Inducement of Gastroenteric Diseases)
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