Helicobacter pylori Cell Biology and Pathogenesis

Dear Colleagues,

It has been more than 38 years since Robin Warren and Barry Marshall have published the results of their studies showing the relationship between H. pylori infection of gastric mucosa and active chronic gastritis, duodenal ulcers and gastric ulcers. This discovery has contributed to our understanding of the general relationship between chronic infection, inflammation and cancer and expanded the search for the microbiological background of other diseases related to chronic inflammation. Indeed, H. pylori has been associated with the development of certain malignancies and classified as a type I carcinogen. Additionally, it has been shown that H. pylori eradication also significantly lowered the risk of gastric cancer in initially healthy, asymptomatic patients, especially when H. pylori was eradicated at early stages of infection. On the other hand, some studies have suggested that, depending on the strain type, H. pylori may play a role in the natural stomach ecology, for example, by influencing the type of bacteria that colonize the gastrointestinal tract, normalize stomach acid secretion, and regulate appetite. Thus, there is a need for more comprehensive studies on the role of H. pylori and host cell interactions, particularly in light of the rising resistance of this bacterium to commonly used antibiotics.

Topics of interest for this Special Issue include, but are not limited to:

• Models of host–microbial persistence;
• H. pylori cell biology (e.g., strain types, virulence factor presence and adaptation mechanisms);
• H. pylori strain types and host interactions:

            -H. pylori–gastric microbiome interactions;

            -H. pylori–immune cell interactions;

            -H. pylori–tissue cell interactions (biochemical, biophysical);

            -H. pylori–stem cell interactions;

            -H. pylori–cancer cell interactions;

• H. pylori-induced physiological processes regulation and dysregulation (e.g., systemic, extra- and intracellular signaling change, gene expression changes (genetic and epigenetic));
• H. pylori pathology (e.g., inflammation, fibrosis, cancer, immunosuppression);
• Host susceptibility;
• H. pylori epidemiology;
• H. pylori and antibiotic resistance;
• H. pylori and cancer prognostic factors;
• Therapeutic approaches like targeted treatment of H. pylori-related pathophysiological tissue-related changes (e.g., new eradication tools, natural and chemical compounds impairing virulence-factor-associated pathogenicity).

Dr. Gracjana Krzysiek-Maczka
Guest Editor

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