Nasal

Background: Nasal Methods: A murine psoriasis model was established using imiquimod (IMQ) and intranasal SP challenge, with disease severity evaluated via PASI scoring and histology, epidermal proliferation (Ki67) and T cell (CD3) via immunofluorescence, immunohistochemistry, and IL-23, IL-17A, and IL-1β levels via enzyme-linked immunosorbent assay (ELISA) in skin. Immune cell infiltration (DCs, γδ T cells) was analyzed by flow cytometry, RNA-seq identified affected genes and pathways, and real-time polymerase chain reaction (qPCR) /Western blot (WB) detected transcription and protein levels of target genes in SP lipoteichoic acid (LTA)-activated BMDCs in vitro. Oxygen consumption rate (OCR), extracellular acidification rate (ECAR), wound healing, Transwell migration, and co-culture assays assessed metabolic reprogramming and migration function of BMDCs in response to LTA in vitro. CD11c-Luc reporter mice were monitored via bioluminescence imaging (BLI) to dynamically track DC migration in vivo, and confocal immunofluorescence co-localization was used to visualize DC-γδT cell interactions in skin. Results: Nasal SP infection exacerbated psoriasis-like lesions by increasing PASI scores (10.3 ± 0.2 in Re-SP vs 8.2 ± 0.4 in Re, Conclusion: These findings suggest that nasal SP infection may exacerbate psoriasis relapse through TLR2-dependent DC metabolic reprogramming and trafficking, which in turn promote γδ T cell IL-17A production. However, as these findings are derived from preclinical mouse models and in vitro experiments, validation in human psoriasis cohorts and chronic disease models is required before clinical translation can be considered.