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嗜酸乳杆菌通过影响调节性T细胞/辅助性T细胞17平衡参与颗粒物诱导的肠道炎症。

L.acidophilus participates in intestinal inflammation induced by PM through affecting the Treg/Th17 balance.

作者信息

Xu Jie, Wang Jing, He Yuefeng, Chen Rui, Meng Qingtao

机构信息

Yunnan Provincial Key Laboratory of Public Health and Biosafety & School of Public Health, Kunming Medical University, Kunming 650500, China.

School of Public Health, Capital Medical University, Beijing 100069, China.

出版信息

Environ Pollut. 2024 Jan 15;341:122977. doi: 10.1016/j.envpol.2023.122977. Epub 2023 Nov 23.

Abstract

Particulate matter with aerodynamic diameters of ≤2.5 μm (PM) is associated with multiple organ damage, among which the influence of PM on the gastrointestinal system has been a recent focus of attention. In this study, four different types of PM exposure models are established to determine the occurrence of PM induced intestinal inflammation. In view of the abnormal expression of lymphocytes detected in the model and the well-known fact that the intestine is the largest immune organ, we focused on the intestinal immune system. A combined regulatory T cell (Treg) transplantation experiment demonstrated that PM induced intestinal inflammation by affecting the imbalance of regulatory T cell/T helper cell 17 (Treg/Th17). Since the intestine has the highest microbial content, and the results of the 16S rDNA third-generation sequencing analysis further revealed that the abundance of Lactobacillus_acidophilus (L.acidophilus) decreased significantly after PM exposure. The following mechanism study confirmed that L.acidophilus participated in an imbalance of Treg/Th17. Moreover, L.acidophilus supplementation successfully alleviated intestinal inflammation by regulated regulating the balance of Treg/Th17 under the background of PM exposure. Hence, this is a potential method to protect against intestinal inflammation induced by PM.

摘要

空气动力学直径≤2.5微米的颗粒物(PM)与多器官损伤有关,其中PM对胃肠系统的影响是近期关注的焦点。在本研究中,建立了四种不同类型的PM暴露模型以确定PM诱导的肠道炎症的发生情况。鉴于在该模型中检测到淋巴细胞的异常表达,且肠道是最大的免疫器官这一众所周知的事实,我们将重点放在肠道免疫系统上。一项联合调节性T细胞(Treg)移植实验表明,PM通过影响调节性T细胞/辅助性T细胞17(Treg/Th17)的失衡来诱导肠道炎症。由于肠道微生物含量最高,16S rDNA第三代测序分析结果进一步显示,PM暴露后嗜酸乳杆菌(L.acidophilus)的丰度显著降低。随后的机制研究证实,嗜酸乳杆菌参与了Treg/Th17的失衡。此外,在PM暴露背景下,补充嗜酸乳杆菌通过调节Treg/Th17的平衡成功减轻了肠道炎症。因此,这是一种预防PM诱导的肠道炎症的潜在方法。

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