Evidence map›Paper›PMID 42382776›Full record

ArticleFrontiers in immunology2026

Electroacupuncture as an eosinophil-targeting treatment in ovalbumin-induced allergic rhinitis involving β

Tran Van Bao Quach, Thanh-Hien Vu Nguyen, Ngoc Chi Lan Nguyen, Che-Hsuan Lin, Yi-Hung Chen

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Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Tran Van Bao QuachGraduate Institute of Acupuncture Science, China Medical University, Taichung, Taiwan.
Thanh-Hien Vu NguyenGraduate Institute of Acupuncture Science, China Medical University, Taichung, Taiwan.
Ngoc Chi Lan NguyenFaculty of Traditional Medicine, Can Tho University of Medicine and Pharmacy, Can Tho, Vietnam.
Che-Hsuan LinDepartment of Otolaryngology, School of Medicine, College of Medicine, Taipei Medical University (TMU), Taipei, Taiwan.
Yi-Hung ChenGraduate Institute of Acupuncture Science, China Medical University, Taichung, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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 β 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 β

Indexed as

ElectroacupunctureEosinophilsReceptors, Adrenergic, beta-2Rhinitis, AllergicAnimalsCytokinesDisease Models, AnimalFemaleImmunoglobulin EMast CellsMiceMice, Inbred BALB COvalbuminCytokinesImmunoglobulin EOvalbuminReceptors, Adrenergic, beta-2allergic rhinitiselectroacupunctureeosinophilsepinephrinenorepinephrineβ2 adrenergic receptors

Identifiers

PMID42382776
PMCPMC13314418

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.