Frontiers in immunology · 2026
Electroacupuncture as an eosinophil-targeting treatment in ovalbumin-induced allergic rhinitis involving β2-adrenergic receptor in a mouse model.
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Quach Tran Van Bao, Nguyen Thanh-Hien Vu, Nguyen Ngoc Chi Lan, Lin Che-Hsuan, Chen Yi-Hung
Аннотация
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.
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.