Fig 1: Chronic exposure to SA‐EVs induces sustained gastric inflammation. (A) BALB/c female mice (n=6 per group) were orally gavaged with either SA‐EVs, H. pylori or PBS for two months. (B) Representative fluorescence in situ hybridization (FISH) images of gastric tissue sections from mice gavaged with SA‐EVs or PBS at two months post‐infection. (Blue indicates nuclei; green indicates S. anginosus probe). Scale bars represent 50 µm. (C) Representative hematoxylin and eosin (H&E) staining images of stomach tissue from mice treated with SA‐EVs, H. pylori or PBS at two months post‐infection. Scale bars=50 µm. (D) Gastric inflammation scores for the different groups: score 0, no inflammation; score 1, mild inflammation; score 2, moderate inflammation; score 3, severe inflammation; score 4, critical inflammation. (E‐M) Serum levels of IL‐17A, CCL20, IL‐6, IL‐12, CCL8, and TNF‐a, were upregulated following SA‐EVs infection at two weeks post‐infection. (L–O) Flow pattern(O) and statistical analysis(L‐N) of IL‐22, IL‐17A, and TNF‐α in gastric tissue following 3 months of intragastric administration. (P) ELISA analysis of TNF‐α, IL‐17a, CCL20, and IL‐1β in gastric tissue following 3 months of intragastric administration. Data is shown as mean ± SD, with dots representing individual donors (average of technical duplicates, n = 6). Statistical differences between groups were determined using one‐way ANOVA with Tukey post‐tests. p < 0.05 (*); p < 0.01 (**); p < 0.001 (***); p < 0.0001 (****); ns: not significant.