ArticleEuropean archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery2025
Staphylococcus aureus regulates Th17 cells and autophagy via STING in chronic eosinophilic rhinosinusitis with nasal polyps.
Article in European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Research progress on T-cell responses inFrontiers in microbiology · 2026Pooled it
- Beyond Pathogens: Modulating the Commensal Microbiota to Reshape Immunity for Respiratory Disease Intervention.Pathogens (Basel, Switzerland) · 2026Review
- Multi-Omics Insights into Chronic Rhinosinusitis with Nasal Polyps: A Review of Lipidomics, Proteomics, and Transcriptomics.Journal of inflammation research · 2026Review
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4 authors.
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Abstract
purposeAs a common pathogen of rhinosinusitis, the role of Staphylococcus aureus in modulating autophagy through STING activation and Th17 cell differentiation in CRSwNP remains unexplored. This study aims to investigate how S. aureus regulates Th17 cell differentiation and the occurrence and development of autophagy in CRS by inducing STING expression.
methodsImmunoblotting and flow cytometry were employed to assess the expression levels of STING, RORγt, LC3B, and MUC5AC, as well as Th17 markers in cells. HNECs were co-cultured with S. aureus in vitro to explore its regulatory effects.
resultsSTING expression was found to be decreased in CRSwNP tissues, while RORγt, LC3B, and MUC5AC levels were elevated. S. aureus was shown to induce Th17 differentiation via STING regulation. STING activators reduced Th17 inflammation, while autophagy activators increased autophagosomes and MUC5AC levels.
conclusionThe STING system may play a protective role in the inflammatory response of nasal epithelial cells. S. aureus inhibits STING, not only by promoting the differentiation of pathogenic Th17 cells but also by increasing autophagy levels in nasal epithelial cells. Both mechanisms contribute to the enhanced expression of MUC5AC, facilitating the progression of CRSwNP.
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