Electroacupuncture targets β2-adrenergic receptors to reduce eosinophilic inflammation in allergic rhinitis mice

Eosinophils are key drivers of type-2 (Th2) inflammation and tissue injury in allergic rhinitis (AR), with their burden correlating with disease severity and asthma risk. Current AR therapies often have limitations, prompting interest in non-pharmacologic interventions like neuromodulation. This study investigates whether electroacupuncture (EA) can attenuate eosinophilic inflammation in AR and explores the underlying neuroimmune mechanisms, specifically focusing on the sympathetic nervous system's role.

Researchers used an ovalbumin (OVA)-induced AR mouse model to compare electroacupuncture (EA) with the antihistamine chlorpheniramine (CLP). They assessed nasal behaviors (rubbing, redness, olfactory dysfunction), inflammatory biomarkers (IL-5, IL-13, OVA-specific IgE, RNASE2A, MCPT1), and histological changes (eosinophil infiltration, mast cell degranulation). Mechanistic studies involved pre-administering β2-adrenergic antagonist butoxamine or dopamine D1 antagonist butaclamol before EA, followed by plasma catecholamine measurements and intranasal epinephrine rescue experiments.

In OVA-challenged mice, EA significantly alleviated nasal rubbing, redness, and olfactory dysfunction, demonstrating 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, strongly implicating β2-adrenergic receptor activation.