Staphylococcus aureus regulates Th17 cells and autophagy via STING in chronic eosinophilic rhinosinusitis with nasal polyps.

Abstract

Purpose: As 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.

Methods: Immunoblotting 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.

Results: STING 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.

Conclusion: The 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.