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Updated: Jun 29, 2025

Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226
Published on: May 10, 2022
IL-6 mediates olfactory dysfunction in a mouse model of allergic rhinitis
Xiao-Yu Song1, Qi Sun1, Shi-Zhuang Wei1
1Department of Otorhinolaryngology, Head and Neck Surgery, Yantai Yuhuangding Hospital, Qingdao University, Yantai, China; Shandong Provincial Clinical Research Center for Otorhinolaryngologic Diseases, Yantai Yuhuangding Hospital, Yantai, China; Yantai Key Laboratory of Otorhinolaryngologic Diseases, Yantai Yuhuangding Hospital, Yantai, China.
Interleukin-6 (IL-6) drives olfactory dysfunction (OD) in allergic rhinitis (AR) by promoting neuroinflammation in the olfactory bulb. Targeting IL-6 may offer a new therapeutic strategy for AR-related OD.
Area of Science:
- Immunology
- Neuroscience
- Otorhinolaryngology
Background:
- Immune-inflammatory responses are central to olfactory dysfunction (OD) in allergic rhinitis (AR).
- Interleukin-6 (IL-6), a key inflammatory mediator, is implicated in allergic diseases and other conditions causing OD.
- The specific role of IL-6 in AR-related OD remains uninvestigated.
Purpose of the Study:
- To investigate the role of IL-6 in the development of OD in AR.
- To identify IL-6 as a potential therapeutic target for AR-associated OD.
Main Methods:
- Differential gene expression analysis of AR datasets (GSE52804, GSE140454) and the General Olfactory Sensitivity Database (GOSdb).
- Development of an AR mouse model with OD induced by ovalbumin (OVA) sensitization.
- In vitro co-culture models using nasal mucosa epithelial cells and microglia stimulated with Derp1 allergen extract.
Main Results:
- Elevated IL-6 levels in the nasal mucosa and olfactory bulbs of AR mice with OD, correlating with microglia activation (Iba-1) and OD severity.
- Allergen stimulation of nasal epithelial cells increased IL-6, decreased barrier function, and promoted microglial neuroinflammation (IL-1β, iNOS).
- Knockdown of IL-6 receptor (IL-6R) using siRNA significantly reduced neuroinflammatory marker expression.
Conclusions:
- IL-6 plays a critical role in the pathogenesis of OD in AR.
- IL-6-induced neuroinflammation, mediated by olfactory bulb microglia, is a key mechanism underlying AR-related OD.
- IL-6 presents a promising therapeutic target for managing OD in AR patients.

