Acupuncture inhibited airway inflammation and group 2 innate lymphoid cells in the lung in an ovalbumin-induced murine asthma model

医学 先天性淋巴细胞 卵清蛋白 免疫学 炎症 哮喘 针灸科 支气管肺泡灌洗 免疫系统 先天免疫系统 内科学 病理 替代医学
作者
Jie Cui,Ming Dong,La Yi,Ying Wei,Weifeng Tang,Xueyi Zhu,Jingcheng Dong,Wenqian Wang
出处
期刊:Acupuncture in Medicine [SAGE Publishing]
卷期号:39 (3): 217-225 被引量:8
标识
DOI:10.1177/0964528420924033
摘要

Background Group 2 innate lymphoid cells (ILC2s) are known to serve important functions in the pathogenesis of allergic airway inflammation. Studies have shown that acupuncture has an anti-inflammatory effect in the airways. However, how acupuncture treatment affects innate immunity, especially with regard to the function of ILC2s in ovalbumin (OVA)-induced allergic airway inflammation, is poorly understood. Methods BALB/c mice were injected and subsequently challenged with OVA ± treated with manual acupuncture. At the end of the experimental course, lung function was assessed by measurement of airway resistance (R L ) and lung dynamic compliance (Cdyn). Cytokine levels were detected by enzyme-linked immunosorbent assay (ELISA). ILC2 proportions in the lung were analyzed by flow cytometry. Results The results showed that airway inflammation and mucus secretion were significantly suppressed by acupuncture treatment. R L decreased while Cdyn increased after acupuncture treatment. There was an apparent decrease in the bronchoalveolar lavage fluid (BALF) concentrations of interleukin (IL)-5, IL-13, IL-9, IL-25 and IL-33 and an increase in soluble IL-33 receptor (sST2) levels compared with untreated asthmatic mice. Acupuncture also reduced the lin – CD45 + KLRG1 + ST2 + cell proportion in the lung. Conclusion In conclusion, this study has demonstrated that acupuncture treatment alleviates allergic airway inflammation and inhibits pulmonary ILC2 influx and IL-5, IL-9 and IL-13 production. The inhibition of ILC2s by acupuncture may be associated with the IL-33/ST2-signaling pathway and IL-25 levels, thereby offering protection from the respiratory inflammation associated with asthma.
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