Kechuanting Acupoint Sticking Therapy Alleviates Type 2 Airway Inflammation in Mice with Allergic Asthma by...

Kechuanting Acupoint Sticking Therapy (KAST) has been shown to effectively improve airway inflammation in patients with allergic asthma (AA); however, its underlying mechanisms remain unclear. This study aimed to investigate the therapeutic mechanisms of KAST in an AA mouse model from a neuro-immune perspective. An ovalbumen (OVA)-induced allergic asthma mouse model was established, and the mice were treated with KAST. The effects of KAST on pulmonary Group 2 innate lymphoid cells (ILC2s) and type 2 airway inflammation were evaluated using flow cytometry, hematoxylin-eosin (HE) staining, and immunohistochemistry. Western blotting (WB) and ELISA were used to assess calcitonin gene-related peptide (CGRP) protein levels in lung tissues. Intranasal administration of CGRP or the CGRP receptor inhibitor BIBN-4096 was performed in mice with allergic asthma to investigate the regulatory role of the CGRP/receptor activity-modifying protein 1 (RAMP1) pathway on ILC2s and type 2 airway inflammation. KAST reduced the number of ILC2s and alleviated type 2 airway inflammation, accompanied by decreased CGRP expression in lung tissues. Intranasal CGRP increased RAMP1⁺ILC2s and total ILC2s in the lungs and exacerbated type 2 airway inflammation. Conversely, intranasal BIBN-4096 decreased pulmonary ILC2s and mitigated type 2 airway inflammation. KAST reduces airway inflammation in allergic asthma, which is closely associated with downregulation of the CGRP/RAMP1 pathway and subsequent suppression of pulmonary ILC2s, as supported by pharmacologic inhibition.