The major component of the gastric microbiota in around half of the world’s population is the Proteobacteria Helicobacter pylori; a fastidious, microaerophilic microorganism characterized by a high geographic variability. H. pylori is the causative agent of many gastric diseases for instance gastritis, peptic and duodenal ulcer, gastric mucosa-associated lymphoid tissue (MALT) lymphoma or gastric cancer. Several studies demonstrated that the gut microbiota could be affected by the colonization of H. pylori and that the association between this colonization and an altered gastric microbiota induces the development of gastric diseases.
Moreover, it has been widely suggested that the eradication of H. pylori infection represents a useful strategy for preventing gastric cancer, although some studies concluded that the gastric mucosa colonization of non-H. pylori bacteria can also represent a risk factor for the development of gastric cancer.
It is currently not clear whether the colonization of H. pylori promotes the dysbiosis or, inversely, an altered microbiota creates a suitable condition for H. pylori colonization, survival and persistence. Multiple host and bacterial factors certainly interact with each other, affecting the composition and function of the gut microbiota as well as the development of severe gastric diseases. The likelihood of clinical sequelae has been associated with the production of virulence factors, such as the cytotoxin-associated gene A (CagA) and the VacA cytotoxin. Virulence factors can be externally secreted and introduced to a host cell by the type IV secretion system or by Outer Membrane Vesicles (OMVs), spherical lipidic structures produced by H. pylori as a strategy to support its survival in the gastric mucosa.
The survival and persistence of H. pylori in the host and environment is also enabled by its high genetic diversity and variability as well as by its extraordinary adaptability to stressful conditions through the production of biofilm and/or the conversion in the viable but non- culturable (VBNC) state. Furthermore, the increasing antibiotic resistance reported in H. pylori, versus the recommended treatment therapies, supports the need to identify new eradication strategies.
The aim of the present Research Topic is to create a collection of articles focalized on the following:
(i) role of H. pylori in the gastric inflammation and development of severe gastric diseases, particularly cancer; its virulence and pathogenesis demonstrated by the production of virulence factors, biofilm formation, the VBNC state, and the release of OMVs;
(ii) impact of the microbiota on the development of gastric diseases as well as the impact of Helicobacter pylori on gut microbiota/microbiome composition;
(iii) identification of innovative strategies, including the use of probiotics, for the eradication of Helicobacter pylori in order to recover the eubiosis.
Encouraged are submissions of Original Research articles, Commentaries, Review articles, Opinion articles, or Hypothesis and Theory articles.
The major component of the gastric microbiota in around half of the world’s population is the Proteobacteria Helicobacter pylori; a fastidious, microaerophilic microorganism characterized by a high geographic variability. H. pylori is the causative agent of many gastric diseases for instance gastritis, peptic and duodenal ulcer, gastric mucosa-associated lymphoid tissue (MALT) lymphoma or gastric cancer. Several studies demonstrated that the gut microbiota could be affected by the colonization of H. pylori and that the association between this colonization and an altered gastric microbiota induces the development of gastric diseases.
Moreover, it has been widely suggested that the eradication of H. pylori infection represents a useful strategy for preventing gastric cancer, although some studies concluded that the gastric mucosa colonization of non-H. pylori bacteria can also represent a risk factor for the development of gastric cancer.
It is currently not clear whether the colonization of H. pylori promotes the dysbiosis or, inversely, an altered microbiota creates a suitable condition for H. pylori colonization, survival and persistence. Multiple host and bacterial factors certainly interact with each other, affecting the composition and function of the gut microbiota as well as the development of severe gastric diseases. The likelihood of clinical sequelae has been associated with the production of virulence factors, such as the cytotoxin-associated gene A (CagA) and the VacA cytotoxin. Virulence factors can be externally secreted and introduced to a host cell by the type IV secretion system or by Outer Membrane Vesicles (OMVs), spherical lipidic structures produced by H. pylori as a strategy to support its survival in the gastric mucosa.
The survival and persistence of H. pylori in the host and environment is also enabled by its high genetic diversity and variability as well as by its extraordinary adaptability to stressful conditions through the production of biofilm and/or the conversion in the viable but non- culturable (VBNC) state. Furthermore, the increasing antibiotic resistance reported in H. pylori, versus the recommended treatment therapies, supports the need to identify new eradication strategies.
The aim of the present Research Topic is to create a collection of articles focalized on the following:
(i) role of H. pylori in the gastric inflammation and development of severe gastric diseases, particularly cancer; its virulence and pathogenesis demonstrated by the production of virulence factors, biofilm formation, the VBNC state, and the release of OMVs;
(ii) impact of the microbiota on the development of gastric diseases as well as the impact of Helicobacter pylori on gut microbiota/microbiome composition;
(iii) identification of innovative strategies, including the use of probiotics, for the eradication of Helicobacter pylori in order to recover the eubiosis.
Encouraged are submissions of Original Research articles, Commentaries, Review articles, Opinion articles, or Hypothesis and Theory articles.