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        <identifier>oai:figshare.com:article/33964294</identifier>
        <datestamp>2026-09-22T11:00:02Z</datestamp>
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          <dc:title>Table 1_The oral-gastric microbial axis in children: salivary signatures as non-invasive biomarkers for pediatric gastritis and Helicobacter pylori infection.docx</dc:title>
          <dc:creator>Ji Hyun Seo (15152634)</dc:creator>
          <dc:creator>Ji Sook Park (8776388)</dc:creator>
          <dc:creator>Jung Je Park (2605534)</dc:creator>
          <dc:creator>Young-Sool Hah (518983)</dc:creator>
          <dc:subject>Clinical Microbiology</dc:subject>
          <dc:subject>oral-gastric axis</dc:subject>
          <dc:subject>pediatric gastritis</dc:subject>
          <dc:subject>Helicobacter pylori</dc:subject>
          <dc:subject>salivary microbiome</dc:subject>
          <dc:subject>non-invasive biomarkers</dc:subject>
          <dc:subject>oral microbiome</dc:subject>
          <dc:subject>dysbiosis</dc:subject>
          <dc:description>&lt;p&gt;Helicobacter pylori is commonly acquired in childhood, with the mouth a presumed portal of entry, although the relative contributions of oral-oral, gastro-oral, and fecal-oral transmission remain unresolved. It is a principal cause of pediatric gastritis, yet most infected children are asymptomatic, and the pediatric mucosa mounts a tolerogenic response rather than the aggressive inflammation seen in adults. In the pathway defined by pediatric guidelines, diagnosis depends on endoscopy with multiple gastric biopsies, an invasive reference standard not suitable for serial assessment; non-invasive tests are reserved largely for confirming eradication and have age-specific limitations in young children. This narrative review, supported by a structured literature search, develops the oral-gastric microbial axis as an organizing framework for non-invasive pediatric assessment, on the premise—not yet demonstrated longitudinally—that early oral colonization shapes later gastric disease: the two compartments are ecologically continuous, and acid-tolerant oral bacteria that survive gastric transit provide a pro-inflammatory metabolic input to the mucosa. We evaluate candidate salivary and oral signatures—taxonomic, H. pylori-specific, and metabolic—and grade each on two axes: the population generating the evidence (pediatric, adult, or non-human) and the stage of biomarker development reached, each tied to a stated target condition. The picture is asymmetric: the connectivity argument is well supported and the mechanistic account coherent, but the model has not been demonstrated end-to-end in children. A few signatures have genuine pediatric support, and salivary assays targeting the H. pylori 23S rRNA gene reach the clinical-assay stage on pediatric evidence, with sensitivity of 87-94% but specificity ranging from 80% to 100% in the two cohorts with recoverable two-by-two data; no candidate has been independently validated in children, most evidence is adult-derived, and whether the oral cavity is a true H. pylori reservoir remains unresolved. Because a single, unreplicated comparative study indicates that H. pylori remodels the gastric microbiota differently in children than in adults, adult signatures cannot be assumed transferable. We conclude that oral-gastric signatures currently suit research stratification rather than clinical decision-making, and specify the longitudinal, multi-omics, viability-resolved studies needed to advance them toward clinical validity.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-22T11:00:02Z</dc:date>
          <dc:type>Dataset</dc:type>
          <dc:type>Dataset</dc:type>
          <dc:identifier>10.3389/fcimb.2026.1934250.s001</dc:identifier>
          <dc:relation>https://figshare.com/articles/dataset/Table_1_The_oral-gastric_microbial_axis_in_children_salivary_signatures_as_non-invasive_biomarkers_for_pediatric_gastritis_and_Helicobacter_pylori_infection_docx/33964294</dc:relation>
          <dc:rights>CC BY 4.0</dc:rights>
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