Helicobacter (H) pylori is a Gram-negative bacterium that colonizes the gastric mucosa of about 50% of the human population. This microorganism has accompanied humans since the beginning of our species and has coevolved with us to become the main bacterial species of the microbiome in the stomach. We have learned that its presence is important to modulate the activity of immune cells, particularly T regulatory cells, and has a role in preventing autoimmune diseases such as asthma or allergies. H. pylori grows efficiently deep in the gastric glands in harmony with cells in the epithelia. Unfortunately, a small fraction of the colonized individuals, less than 3%, will develop gastric cancer decades after the initial colonization early in life.
Understanding why this bacteria-host interaction could lead to tissue damage and eventually to gastric cancer development is a major challenge. Although a full picture of the molecular mechanism by which H. pylor induces carcinogenesis is still elusive, we know that it can activate a number of cellular pathways that may trigger chronic uncontrolled inflammation in the gastric mucosa, disrupt cellular autophagy, cause aberrant DNA methylation or altered the expression of regulatory oncogenes. Recent studies suggest that the co-ancestry of H. pylori and its human host plays an important role in the outcome of the relationship; and when the ancestry of the colonizing bacteria does not match the ancestry of its host, the risk of tissue damage increases.
Randomized clinical trials conducted in high-risk populations for gastric cancer using various anti-H. pylori regimens have shown that H. pylori eradication decreases gastric cancer incidence in healthy populations as well as the risk of the 2nd metachronous gastric cancer in patients with a history of gastric cancer. However, the screening and eradication of H. pylori is not always a viable option, especially in low-mid income counties where H. pylori prevalence is high, and thus targeting H. pylori dependent carcinogenic pathways is a crucial strategy to fight against gastric cancer.
The aim of this Research Topic is to present new insights that contribute to the understanding of the mechanisms that govern the gastric neoplastic transformation induced by H. pylori infection.
We welcome manuscripts focused on, but not limited to:
- Changes in immune and/or gastric epithelial cells responses
- H. pylori-induced changes in the microbiome related to gastric cancer
- H. pylori-induced metabolic changes in gastric mucosa
- Alterations of cell signaling pathways
- Oncogene activation and mechanism of action in response to H. pylori infection
- Characterization of new or understudied H. pylori virulence factors.
- In vivo evolution of H. pylori colonization
- Interaction between H. pylori infection or its virulence factors and host genetic and behavioral risk factors
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Helicobacter (H) pylori is a Gram-negative bacterium that colonizes the gastric mucosa of about 50% of the human population. This microorganism has accompanied humans since the beginning of our species and has coevolved with us to become the main bacterial species of the microbiome in the stomach. We have learned that its presence is important to modulate the activity of immune cells, particularly T regulatory cells, and has a role in preventing autoimmune diseases such as asthma or allergies. H. pylori grows efficiently deep in the gastric glands in harmony with cells in the epithelia. Unfortunately, a small fraction of the colonized individuals, less than 3%, will develop gastric cancer decades after the initial colonization early in life.
Understanding why this bacteria-host interaction could lead to tissue damage and eventually to gastric cancer development is a major challenge. Although a full picture of the molecular mechanism by which H. pylor induces carcinogenesis is still elusive, we know that it can activate a number of cellular pathways that may trigger chronic uncontrolled inflammation in the gastric mucosa, disrupt cellular autophagy, cause aberrant DNA methylation or altered the expression of regulatory oncogenes. Recent studies suggest that the co-ancestry of H. pylori and its human host plays an important role in the outcome of the relationship; and when the ancestry of the colonizing bacteria does not match the ancestry of its host, the risk of tissue damage increases.
Randomized clinical trials conducted in high-risk populations for gastric cancer using various anti-H. pylori regimens have shown that H. pylori eradication decreases gastric cancer incidence in healthy populations as well as the risk of the 2nd metachronous gastric cancer in patients with a history of gastric cancer. However, the screening and eradication of H. pylori is not always a viable option, especially in low-mid income counties where H. pylori prevalence is high, and thus targeting H. pylori dependent carcinogenic pathways is a crucial strategy to fight against gastric cancer.
The aim of this Research Topic is to present new insights that contribute to the understanding of the mechanisms that govern the gastric neoplastic transformation induced by H. pylori infection.
We welcome manuscripts focused on, but not limited to:
- Changes in immune and/or gastric epithelial cells responses
- H. pylori-induced changes in the microbiome related to gastric cancer
- H. pylori-induced metabolic changes in gastric mucosa
- Alterations of cell signaling pathways
- Oncogene activation and mechanism of action in response to H. pylori infection
- Characterization of new or understudied H. pylori virulence factors.
- In vivo evolution of H. pylori colonization
- Interaction between H. pylori infection or its virulence factors and host genetic and behavioral risk factors
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
