Fig 1: Bacterial induction of DPP4 amplifies immune–epithelial responses in recurrent aphthous stomatitis. A–C Helper T cells segregated into CXCR3⁻ (A), CXCR3⁺ (B), and CXCR3^hi (C) subsets, with DPP4 expression highest in the pro-inflammatory CXCR3^hi population. D–E Streptococcus pneumoniae infection of oral keratinocytes increased DPP4⁺ cells from ~ 0.4% under basal conditions (D) to ~ 36% after infection (E) (p ≤ 0.05). F Pathway enrichment in infected keratinocytes highlighted cytoskeletal remodeling, keratinization, IL-33 signaling, and apoptosis. G Differential protein analysis revealed enrichment of DNA damage responses, adherens junction destabilization, and neuronal-like guidance pathways, consistent with epithelial stress. Together, these results show that Streptococcus pneumoniae exposure under experimental conditions induces epithelial stress responses and inflammation through DPP4 induction, thereby coupling immune and epithelial compartments in a feed-forward loop that may underlie disease recurrence
Fig 2: Immune remodeling in recurrent aphthous stomatitis. A–C Volcano plots of the cellular (pellet) fraction show robust complement system enrichment during ulceration (A), incomplete normalization with selective CD59 upregulation during the ulcerative-to-remission transition (B), and persistent complement activity in remission compared with healthy controls (C). Volcano plots reflect differential protein abundance; therefore, these observations are interpreted as complement-related protein enrichment rather than direct functional activation. D–E Profile plots (D) and multivariate analysis (E) confirm that complement proteins remain elevated in ulcerative and remission stages. These separations are based on pooled samples and represent group-level patterns. F By contrast, soluble (supernatant) measurements of C3a, C4a, and C5a showed no differences between groups. The absence of differences in soluble complement fragments further supports the distinction between protein abundance and functional activation. G Alluvial mapping of supernatant proteins highlights DPP4 as a central hub for chemokine interactions during ulceration, despite unchanged soluble DPP4 levels by ELISA (H). Network centrality reflects inferred connectivity within the dataset. Together, these findings point to a dual immune architecture: complement dysregulation in the cellular fraction and DPP4-mediated chemokine signaling in the soluble fraction. This architecture represents an integrative interpretation of proteomic and immunological data and should be considered hypothesis-generating
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