Kechuanting Acupoint Sticking Therapy Alleviates Type 2 Airway Inflammation in Mice with Allergic Asthma by Modulating the Number of ILC2s.

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.