Electroacupuncture as an eosinophil-targeting treatment in ovalbumin-induced allergic rhinitis involving β2-adrenergic receptor in a mouse model

BackgroundEosinophils amplify type-2 (Th2) inflammation and tissue injury in allergic rhinitis (AR), and eosinophilic burden correlates with disease severity and future asthma risk. Current AR therapies have limitations, motivating interest in non-pharmacologic neuromodulatory approaches.

Here, we tested whether electroacupuncture (EA) attenuates eosinophilic inflammation in AR and probed a candidate neuroimmune mechanism.MethodsUsing an ovalbumin (OVA)-induced AR mouse model, we compared EA with the antihistamine chlorpheniramine (CLP). We assessed nasal behaviors, inflammatory biomarkers, and histological changes.

Mechanistic exploration involved administering β2-adrenergic (butoxamine) or dopamine D1 (butaclamol) antagonists before EA, followed by plasma catecholamine measurements and intranasal epinephrine rescue.ResultsIn OVA-challenged mice, EA significantly alleviated nasal rubbing, redness, and olfactory dysfunction, showing comparable efficacy to CLP. While OVA induction increased IL-5, IL-13, and serum OVA-specific IgE, both treatments significantly reduced these markers.

Crucially, only EA reversed OVA-induced nasal eosinophil infiltration and suppressed RNASE2A expression; CLP primarily suppressed mast cell degranulation and MCPT1 expression. Mechanistically, pre-treatment with butoxamine—but not butaclamol—abolished the EA-mediated reduction of OVA-induced IL-5, IL-13, RNASE2A, and CCR4.

Furthermore, EA was associated with elevated plasma norepinephrine and epinephrine levels.