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Updated: Feb 24, 2026
Super-Resolution Imaging of Bacterial Secreted Proteins Using Genetic Code Expansion
Published on: February 10, 2023
Staphylococcal superantigen-specific IgE reveals functional superantigen production beyond Staphylococcus aureus in
Yuling Zhang1, Yingyue Liu1, Shujian Zhang1
1Beijing Laboratory of Allergic Diseases and Beijing Key Laboratory of New Medicine and Diagnostic Technology Research for Nasal Disease, Beijing Institute of Otolaryngology, Beijing, China; Department of Otorhinolaryngology Head and Neck Surgery, Capital Medical University, Beijing, China; Department of Allergy, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Background:
Staphylococcal superantigen-specific IgE (SAg-IgE) correlates with disease severity in patients with type 2 (T2) chronic rhinosinusitis with nasal polyps (CRSwNP). Although Staphylococcus aureus is recognized as a primary source of SAgs, SAg-IgE is detected even in patients with culture-negative S aureus.
Objective:
We sought to identify the source of SAgs in SAg-IgE-positive patients with T2 CRSwNP with culture-negative S aureus.
Methods:
Metagenomic sequencing was conducted in patients with T2 CRSwNP with repeatedly negative S aureus cultures, stratified by SAg-IgE status. We screened clinical isolates for SAg genes and evaluated SAg functionality by measuring SAg-specific T-cell receptor repertoire expansion and T2 inflammatory responses in an ex vivo infection model.
Results:
The SAg-IgE-positive group showed significantly higher abundances of S epidermidis, S aureus, Lysinibacillus xylanilyticus, and S capitis compared with the SAg-IgE-negative group. Interestingly, in all participants in whom S aureus was detected, S capitis was also present, albeit at low abundance. Redundancy analysis demonstrated clustering of the Staphylococcus genus, SAg-IgE, and IL-5, supporting a potential link between the Staphylococcus genus and SAg-driven immune responses. Notably, a clinical S capitis isolate carried SEA (staphylococcal enterotoxin A) and SEC genes and secreted functional SAgs, which triggered the clonal expansion of SEA/SEC-specific T-cell receptors and exacerbated the T2 inflammatory response via IL-33 induction.
Conclusions:
Metagenomic sequencing reveals that S capitis, beyond S aureus, produces functional SAg to drive T2 response in SAg-IgE-positive patients with CRSwNP when conventional cultures fail to detect S aureus. Independent of culturable bacterial load, tissue SAg-IgE positivity reliably indicates bacterial colonization and SAg exposure in CRSwNP.
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