ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Extracellular Vesicles of Streptococcus anginosus Mediate Gastritis via Epithelial Barrier Disruption and Macrophage-driven Inflammation.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Efficacy of adjuvant chemotherapy in patients with late-onset stage II/III colon cancer: a retrospective cohort study.Open medicine (Warsaw, Poland) · 2026Article
- Article
- From commensal to pathogen: recent advances in the pathogenicity and clinical implications ofFrontiers in microbiology · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
13 authors.
Funding
Abstract
Recent studies suggest Streptococcus anginosus (SA) contributes to gastric disease beyond Helicobacter pylori, yet its pathogenic mechanisms remain unclear. This study demonstrates that SA-derived extracellular vesicles (SA-EVs) accumulate in gastric tissue, enter epithelial cells, and induce acute gastritis characterized by neutrophil infiltration and elevated cytokines (TNF-α, IL-6, IL-17A). Chronic exposure leads to sustained inflammation, tight junction disruption (Claudin-18, Occludin, ZO-1), and mucosal damage. Proteomic analysis identified TMPC and FBP62 as virulence-associated proteins enriched in SA-EVs, while transcriptomics revealed activation of macrophage polarization and cytokine-receptor pathways. Metabolomic profiling indicated dysregulated aspartate metabolism and inflammation-related metabolic changes, alongside increased gut SA abundance. Notably, genetic deletion of Tmpc or Fbp62 significantly attenuated SA-EVs pathogenicity in vivo, reducing gastric inflammation, cytokine production, and macrophage infiltration. These findings establish SA-EVs as key mediators of non-H. pylori gastritis, with TMPC and FBP62 orchestrating epithelial barrier disruption, immune activation, and metabolic dysregulation, highlights their potential as therapeutic targets.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.