Gastric adenocarcinoma is the third leading cause of cancer-related death worldwide, accounting for more than 720,000 deaths annually . The strongest known risk factor for this devastating disease is infection with Helicobacter pylori, which drives the development of premalignant lesions (such as gastric atrophy, intestinal metaplasia, and dysplasia) that can lead to gastric cancer (Fig 1). However, although H. pylori is the most common bacterial infection worldwide and colonizes greater than 50% of the global population, only 1%–3% of infected individuals ever develop gastric cancer.
Drivers of susceptibility to gastric carcinogenesis include H. pylori strain-specific virulence determinants, host constituents, and environmental factors. Along with these elements, the microbiota of the stomach may also influence the development of gastric malignancies. The acidic environment of the stomach in conjunction with low levels of cultured bacteria from this site previously led to assumptions that the gastric niche was not able to support a diverse microbial community. However, recent advances in DNA sequencing of conserved ribosomal RNA genes, phylogenetic analyses, and computational methods have uncovered a complex microbiota within the human stomach with the potential for disease induction .
Read At: PLOS Pathogens