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

BACKGROUND

Eosinophils 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.

METHODS

Using 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.

RESULTS

In 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. While butoxamine blocked EA-induced symptom relief and eosinophil reduction, intranasal epinephrine mimicked EA's beneficial effects on these parameters.

CONCLUSIONS

Our findings demonstrate that EA reduces eosinophilic inflammation and AR behaviors associated with the activation of β2-adrenergic receptors. Unlike standard antihistamines that target mast cells, EA engages a sympathetic neuroimmune axis, representing a promising complementary intervention for eosinophil-driven AR.