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. 2026 Sep 22;16:1934250. doi: 10.3389/fcimb.2026.1934250

Figure 4.

Infographic showing a proposed, not demonstrated, three-stage model of how oral bacteria may contribute to pediatric gastric inflammation. Stage 1: saliva and food carry oral bacteria into the stomach, where the acid barrier at pH 1.5 to 3.5 eliminates most cells but acid-tolerant oral genera survive, as transient passengers or ectopic colonizers. Stage 2: enterosalivary nitrate-nitrite-nitric oxide metabolism and H. pylori urease generate output that is protective at physiological levels and mutagenic at dysbiotic levels. Stage 3: a regulatory T-cell-dominated, tolerogenic pediatric response distinct from the adult pattern. Tags mark pediatric, adult, animal, and in-vitro evidence; dashed arrows mark inferred links.

A proposed mechanistic model linking the oral-gastric axis to pediatric gastric inflammation. The model is read left to right and is a proposal for testing, not a demonstrated causal sequence: it is assembled from pediatric human, adult human, animal, gastric-cancer, and in-vitro evidence, and the complete sequence has not been demonstrated longitudinally in children. Stage 1 (translocation and acid-barrier survival): saliva and food carry oral bacteria into the stomach in a constant downflow; the gastric acid barrier (pH 1.5–3.5) eliminates most cells, but acid-tolerant oral genera (Streptococcus, Veillonella, Prevotella) survive, with outcomes ranging from transient passage to ectopic colonization. Stage 2 (gastric metabolism): the enterosalivary nitrate–nitrite–nitric oxide pathway and H. pylori urease generate output that is double-edged—physiological nitric oxide is protective, whereas dysbiotic levels yield N-nitroso compounds and reactive oxygen species. Stage 3 (pediatric tolerogenic immune response): in a single comparative study that has not been independently replicated, H. pylori infection was associated with remodeling of the gastric microbiota in children but not in adults, accompanied by an expanded regulatory T-cell response (FOXP3, IL-10, TGF-β) that is tolerogenic and mostly asymptomatic, while a shared pro-inflammatory axis operating through the CagA protein is comparatively secondary in children; a further inferential contribution from the Fusobacterium nucleatum adhesin FadA is shown, characterized in colorectal rather than gastric carcinogenesis. Solid arrows denote links demonstrated directly in the population identified by the accompanying tag; dashed arrows denote links inferred by extrapolation across population, species, or disease stage, and every arrow between the three stages is dashed because no cross-level transition has been demonstrated. Tags identify the evidence type for each link: P, pediatric human; A, adult human; An, animal; IV, in vitro; where two tags are given, the link rests on both. Animal evidence contributes to the model but is not the sole basis of any single link, so An is defined in the figure key without appearing on an arrow. Taxa and gene symbols are italicized; protein products such as CagA, FadA and FOXP3 are set in roman. NO, nitric oxide; TGF-β, transforming growth factor β; TNF-α, tumor necrosis factor α.