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Peer-reviewedCC BY 4.0Clinical & Translational Immunology

Staphylococcus aureus‐derived xanthine exacerbates allergic rhinitis‐induced olfactory dysfunction through promoting Th17 cell differentiation and IL‐17A production

  • Yue Hu1,2,3,4,5,6
  • Wenjing Wang7
  • Ting Yang1,2,3,4,5,6
  • Xiaoyu Song1,2,3,4,5,6
  • Yao Wang1,2,3,4,5,6
  • Yuanchao Cheng1,2,3,4,5,6
  • Yakui Mou1,2,3,4,5,6
  • Chao Ren2,8,9
  • Xicheng Song1,2,3,4,5,6
9 affiliations
  1. 1Department of Otorhinolaryngology, Head and Neck Surgery, Yantai Yuhuangding Hospital Qingdao University Yantai China
  2. 2Shandong Provincial Key Laboratory of Neuroimmune Interaction and Regulation Yantai China
  3. 3Shandong Provincial Clinical Research Center for Otorhinolaryngologic Diseases Yantai China
  4. 4Shandong Engineering Research Center for Precision Diagnosis and Treatment of Airway Diseases Yantai China
  5. 5Yantai Key Laboratory of Otorhinolaryngologic Diseases Yantai China
  6. 6Yantai Clinical Research Center for Otorhinolaryngologic Diseases Yantai China
  7. 7Center for Clinical Laboratory, Beijing Youan Hospital Capital Medical University Beijing China
  8. 8Department of Neurology, Yantai Yuhuangding Hospital Qingdao University Yantai China
  9. 9Yantai Municipal Key Medical and Health Laboratory of Yantai Yuhuangding Hospital (Interdisciplinary Brain Science and Geriatric Health Laboratory) Yantai China
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Abstract

Objectives: Allergic rhinitis (AR) is frequently accompanied by olfactory dysfunction (OD), yet the role of microbial metabolites in this process remains poorly elucidated. This study aimed to investigate how xanthine, a metabolite derived from Staphylococcus aureus (Sa), exacerbates AR‐induced OD by promoting Th17 cell differentiation and IL‐17A production.

Methods: Multi‐omics analyses, comprising metabolomics, proteomics and 16S rRNA gene sequencing, were performed on AR patients and mouse models with AR. Sa was cultured and key metabolites in its supernatant were detected using untargeted metabolomics. AR mice were nasally challenged with Sa supernatant or xanthine, and comparisons were made with mice with chronic AR and OD. The therapeutic potential of an anti‐IL‐17A neutralising antibody was assessed in AR mice stimulated with Sa supernatant or xanthine.

Results: Purine metabolism was significantly enriched, and xanthine levels were elevated in AR patients and mouse models, particularly those with OD. Airway microbial dysbiosis in AR mice was characterised by increased Staphylococcus abundance, and the Sa infection pathway was enriched in patients with AR. Untargeted metabolomics of Sa supernatant revealed increased xanthine levels and enrichment of purine metabolism. Nasal challenge with Sa supernatant or xanthine significantly exacerbated OD. Mechanistically, xanthine promoted Th17 cell differentiation and IL‐17A production. Notably, IL‐17A neutralisation effectively alleviated xanthine‐exacerbated OD, indicating a pivotal role for the IL‐17A pathway in this process.

Conclusion: Sa‐derived xanthine aggravates AR‐induced OD by driving Th17 cell differentiation and IL‐17A production. These findings highlight the xanthine–IL‐17A pathway as a potential therapeutic target for improving olfactory function in AR.

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Cite

BibTeXRIS
BibTeX
@article{hu2026staphylococcus,
  title = {{Staphylococcus aureus‐derived xanthine exacerbates allergic rhinitis‐induced olfactory dysfunction through promoting Th17 cell differentiation and IL‐17A production}},
  author = {Yue Hu and Wenjing Wang and Ting Yang and Xiaoyu Song and Yao Wang and Yuanchao Cheng and Yakui Mou and Chao Ren and Xicheng Song},
  journal = {Clinical \& Translational Immunology},
  year = {2026},
  month = nov,
  doi = {10.1002/cti2.70127},
  url = {https://doi.org/10.1002/cti2.70127},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Staphylococcus aureus‐derived xanthine exacerbates allergic rhinitis‐induced olfactory dysfunction through promoting Th17 cell differentiation and IL‐17A production
AU  - Yue Hu
AU  - Wenjing Wang
AU  - Ting Yang
AU  - Xiaoyu Song
AU  - Yao Wang
AU  - Yuanchao Cheng
AU  - Yakui Mou
AU  - Chao Ren
AU  - Xicheng Song
PY  - 2026
DA  - 2026/11/01
JO  - Clinical & Translational Immunology
DO  - 10.1002/cti2.70127
UR  - https://doi.org/10.1002/cti2.70127
AB  - Objectives: Allergic rhinitis (AR) is frequently accompanied by olfactory dysfunction (OD), yet the role of microbial metabolites in this process remains poorly elucidated. This study aimed to investigate how xanthine, a metabolite derived from Staphylococcus aureus (Sa), exacerbates AR‐induced OD by promoting Th17 cell differentiation and IL‐17A production.  Methods: Multi‐omics analyses, comprising metabolomics, proteomics and 16S rRNA gene sequencing, were performed on AR patients and mouse models with AR. Sa was cultured and key metabolites in its supernatant were detected using untargeted metabolomics. AR mice were nasally challenged with Sa supernatant or xanthine, and comparisons were made with mice with chronic AR and OD. The therapeutic potential of an anti‐IL‐17A neutralising antibody was assessed in AR mice stimulated with Sa supernatant or xanthine.  Results: Purine metabolism was significantly enriched, and xanthine levels were elevated in AR patients and mouse models, particularly those with OD. Airway microbial dysbiosis in AR mice was characterised by increased Staphylococcus abundance, and the Sa infection pathway was enriched in patients with AR. Untargeted metabolomics of Sa supernatant revealed increased xanthine levels and enrichment of purine metabolism. Nasal challenge with Sa supernatant or xanthine significantly exacerbated OD. Mechanistically, xanthine promoted Th17 cell differentiation and IL‐17A production. Notably, IL‐17A neutralisation effectively alleviated xanthine‐exacerbated OD, indicating a pivotal role for the IL‐17A pathway in this process.  Conclusion: Sa‐derived xanthine aggravates AR‐induced OD by driving Th17 cell differentiation and IL‐17A production. These findings highlight the xanthine–IL‐17A pathway as a potential therapeutic target for improving olfactory function in AR.
SN  - 2050-0068
ER  -