Keywords
Helicobacter pylori
dysbiosis
gastric carcinogénesis
microbial succession
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Abstract
Infection-associated gastric carcinogenesis has traditionally been viewed as the direct consequence of Helicobacter pylori activity. However, accumulating evidence indicates that this process should be understood within a broader ecological framework. The stomach harbors a distinct microbiota of relatively low biomass but significant functional influence, whose structure and metabolic activity depend on the physiological state of the mucosa. In eubiotic conditions, this ecosystem maintains a dynamic balance, but when chronic H. pylori infection alters epithelial architecture, acid secretion, and inflammatory responses, a reconfiguration of the gastric niche is initiated. Progressive hypochlorhydria and tissue remodeling favor a microbial succession in which H. pylori no longer predominates and bacteria of oral and intestinal origin become more prevalent. This transition is also functional: the emerging community displays metabolic, inflammatory, and potentially genotoxic capacities that can sustain a microenvironment conducive to malignant transformation. Together,these findings redefine gastric carcinogenesis as the outcome of prolonged interactions among an initiating pathogen, a functionally active non-Helicobacter pylori microbiota (secondary microbiota), and an epithelium exposed to chronic inflammation.
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