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The following is a summary of “Allergic fungal rhinosinusitis linked to other hyper-IgE syndromes through defective TH17 responses,” published in the November 2024 issue of Allergy and Immunology by Hua Sun et al.
A gene expression analysis compared sinus mucosa from allergic fungal rhinosinusitis (AFRS) and patients suffering from chronic rhinosinusitis with nasal polyp (CRSwNP). Histatin 1 (HTN1) was the most significantly downregulated antimicrobial peptide (AMP) in AFRS.
Researchers conducted a retrospective study to investigate HTN1 downregulation and linked it to defective STAT3 activation in patients with AFRS.
They used RT-PCR to compare AMP expression and a fungistasis assay to assess antifungal activity in sinus secretions. Flow cytometry was employed to characterize TH17/TH22 cells and signal transducer and activator of transcription (STAT) signaling in patients with AFRS, non-AFRS CRSwNP, and healthy controls.
The results showed decreased AMP expression and antifungal activity in AFRS sinus mucosa. IL-22 and IL-22–producing T cells were deficient, while in vitro studies revealed a defect in IL-6/STAT3 signaling. Epithelial cells expressed AMPs when stimulated with IL-22/IL-17, and TH17 cell abundance was normal.
They found that patients with AFRS had a STAT3 activation defect, leading to IL-17/IL-22 cytokine and AMP deficiencies. Their findings supported the evaluation of therapies aimed at enhancing AMP production in AFRS.
Source: sciencedirect.com/science/article/abs/pii/S0091674924007139
