The treatment of Qibai Pingfei Capsule on chronic obstructive pulmonary disease may be mediated by Th17/Treg balance and gut-lung axis microbiota.

The treatment of Qibai Pingfei Capsule on chronic obstructive pulmonary disease may be mediated by Th17/Treg balance and gut-lung axis microbiota.
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芪白平肺胶囊对慢性阻塞性肺疾病的治疗作用可能是通过调节Th 17/Treg平衡和肠-肺轴菌群介导的。

DOI:
10.1186/s12967-022-03481-w
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发表时间:
2022-06-21
影响因子:
7.4
通讯作者:
Dong, Jingcheng
Dong, Jingcheng
中科院分区:
医学2区
文献类型:
--
作者:
Jia, Yu;He, Tiantian;Wu, Di;Tong, Jiabing;Zhu, Jie;Li, Zegeng;Dong, Jingcheng

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慢性阻塞性肺疾病(COPD)是一种流行的、进行性的呼吸系统疾病,已成为全球第三大死亡原因。越来越多的证据表明,肠道和肺部微生物群失调与COPD有关。研究表明,辅助性T细胞(Th)17/调节性T细胞(Treg)失衡与COPD有关。芪白平肺胶囊是我国临床上用于治疗慢性阻塞性肺疾病的中药。然而,QBPF干预对肠道和肺部Th 17/Treg平衡和微生物群的影响仍然知之甚少。将大鼠随机分为正常对照组、模型组和芪痹通方组,每组8只。建立COPD模型4周后,给予QBPF 2周,检测各组大鼠Th 17细胞、Treg细胞及其相关细胞因子、转录因子、肠道菌群和肺菌群的变化。此外,还测定了肠道和肺微生物群之间以及细菌属与肺功能和免疫功能之间的相关性。结果表明,QBPF能改善COPD大鼠肺功能,促进Th 17/Treg的新平衡。同时,QBPF治疗可调节COPD大鼠肠道和肺微生物群的组成,改善群落结构,抑制肠道中粪球菌_2、普雷沃菌_9和布劳特氏菌的相对丰度以及肺中支原体的相对丰度,但增加肠道中普雷沃菌科_UCG_003和肺中Rikenellaceae_RC9_gut_group的相对丰度。此外,肠-肺轴通过肠和肺微生物群之间的显著相关性得到证实。微生物群的功能分析表明,COPD大鼠肠道和肺部的氨基酸代谢发生了改变。斯皮尔曼相关分析进一步丰富了COPD模型大鼠肠道和肺内菌群与肺功能和免疫功能的关系。本研究提示QBPF可能通过维持机体免疫细胞平衡和调节肠-肺轴菌群而发挥治疗作用,为探索COPD的潜在生物标志物和QBPF治疗COPD的可能机制提供参考。在线版本包含补充材料,可通过10.1186/s12967-022-03481-w获得。
Chronic obstructive pulmonary disease (COPD), a prevalent, progressive respiratory disease, has become the third leading cause of death globally. Increasing evidence suggests that intestinal and pulmonary microbiota dysbiosis is associated with COPD. Researchers have shown that T helper (Th) 17/regulatory T (Treg) imbalance is involved in COPD. Qibai Pingfei Capsule (QBPF) is a traditional Chinese medicine used to treat COPD clinically in China. However, the effects of QBPF intervention on the Th17/Treg balance and microbiota in the gut and lung are still poorly understood. This study divided the rats into three groups (n = 8): control, model, and QBPF group. After establishing the model of COPD for four weeks and administering of QBPF for two weeks, Th17 cells, Treg cells, their associated cytokines, transcription factors, and intestinal and pulmonary microbiota of rats were analyzed. Furthermore, the correlations between intestinal and pulmonary microbiota and between bacterial genera and pulmonary function and immune function were measured. The results revealed that QBPF could improve pulmonary function and contribute to the new balance of Th17/Treg in COPD rats. Meanwhile, QBPF treatment could regulate the composition of intestinal and pulmonary microbiota and improve community structure in COPD rats, suppressing the relative abundance of Coprococcus_2, Prevotella_9, and Blautia in the gut and Mycoplasma in the lung, but accumulating the relative abundance of Prevotellaceae_UCG_003 in the gut and Rikenellaceae_RC9_gut_group in the lung. Additionally, gut–lung axis was confirmed by the significant correlations between the intestinal and pulmonary microbiota. Functional analysis of microbiota showed amino acid metabolism was altered in COPD rats in the gut and lung. Spearman correlation analysis further enriched the relationship between the microbiota in the gut and lung and pulmonary function and immune function in COPD model rats. Our study indicated that the therapeutic effects of QBPF may be achieved by maintaining the immune cell balance and regulating the gut-lung axis microbiota, providing references to explore the potential biomarkers of COPD and the possible mechanism of QBPF to treat COPD. The online version contains supplementary material available at 10.1186/s12967-022-03481-w.
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