Tuo Min Ding Chuan Decoction ameliorates OVA-induced allergic lung inflammation in mice via regulating the differentiation of ILC2s in gut and lung
作者单位：School of Life Sciences Beijing University of Chinese Medicine School of Traditional Chinese Medicine Beijing University of Chinese Medicine
会议名称：《第十三届全国免疫学学术大会》
会议日期：2018年
学科分类：1008[医学-中药学(可授医学、理学学位)] 1006[医学-中西医结合] 100602[医学-中西医结合临床] 10[医学]
基 金：supported by National Natural Science Foundation of China(No.81473656)
关 键 词：ILC2s Allergic asthma Tuo Min Ding Chuan Decoction
摘 要：Objective: To find the effect and mechanism of Tuo Min Ding Chuan(TMDC) Decoction on mice with allergic asthma Methods: Twenty Balb/c mice were randomly divided into control group, model group, TMDC Decoction and dexamethasone positive group. Murine asthmatic model was established by i.p. injection of OVA plus Al(OH)3 and i.n. nebulization of OVA. The histopathological assessment and differential cell counts of inflammatory cells from BALF were detected by HE and Diff-quick staining respectively. The amount of ILC2 s from lung and gut was measured by flow ***: It clearly showed that there were plenty of mucus secretion inside the bronchia and a large number of inflammatory cells infiltrating around the bronchia in asthmatic mice. After the treatment of TMDC decoction, inflammatory exudation and mucus secretion was obviously alleviated in the lung from asthmatic mice(p0.05). It’s worth noting that inflammatory cells were simultaneously infiltrated in intestinal lamina propria in model mice. What’s more, both of the amounts of ILC2 from pulmonary and intestinal tissues were increased significantly in asthmatic mice, compared to control(p0.01). TMDC decoction not only inhibited the inflammation of lung and intestine tissues, but also decreased the numbers of ILC2 from lung and gut of asthmatic mice(p0.05).Conclusion: Our data indicated that murine allergic asthma model induced by OVA shows immune damage in both lung and intestine while Tuo Min Ding Chuan decoction has a remarkable effect probably through regulating the differentiation of ILC2 s from gut in asthmatic mice.