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

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• 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