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白细胞介素-10/白细胞介素-10受体1通路促进间质性肺炎组织来源的肺成纤维细胞的活力和胶原蛋白合成。

IL-10/IL-10 receptor 1 pathway promotes the viability and collagen synthesis of pulmonary fibroblasts originated from interstitial pneumonia tissues.

作者信息

Ye Hong, Pan Jiongwei, Cai Xiaoping, Yin Zhangyong, Li Lu, Gong Enhui, Xu Cunlai, Zheng Hao, Cao Zhuo, Chen Enguo, Qian Junfeng

机构信息

Respiratory Department, The Sixth Affiliated Hospital of Wenzhou Medical University/Lishui People's Hospital, Lishui, Zheijang 323000, P.R. China.

Department of Respiratory and Critical Care Medicine, Sir Run Run Shaw Hospital, Affiliated to Zhejiang University School of Medicine, Hangzhou, Zheijang 310016, P.R. China.

出版信息

Exp Ther Med. 2022 Jun 15;24(2):518. doi: 10.3892/etm.2022.11445. eCollection 2022 Aug.

DOI:10.3892/etm.2022.11445
PMID:35837039
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9257754/
Abstract

Interstitial pneumonia is a pulmonary interstitial inflammatory and fibrosis disease with a variety of causes that causes respiratory disorders and threatens the lives of patients. The present study aimed to investigate the expression of interleukin (IL)-10 in peripheral blood of patients with interstitial pneumonia and its biological functions in pulmonary fibroblasts. A total of 42 patients with idiopathic pulmonary fibrosis (IPF) and 20 healthy subjects were included. ELISA was used to determine IL-10 concentration in serum from the patients and healthy subjects. Primary fibroblasts were isolated from lung tissue successfully and determined by morphology. The CCK-8 assay was performed to determine the effect of IL-10 expression on cell viability. Western blotting was used to determine COL1a1, COL1a2 and IL-10R1 protein expression. Flow cytometry was used for cell cycle analysis and to determine the number of IL-10 cells. Expression of IL-10 in serum from IPF patients was higher compared to that from healthy subjects. IL-10 promoted the viability and collagen synthesis and secretion of MRC-5 cells and primary pulmonary fibroblasts. IL-10 and IL-10 receptor (R) 1 served regulatory roles in the viability and collagen synthesis of MRC-5 cells. The ratio of peripheral mononuclear lymphocytes with positive expression of IL-10 was elevated in peripheral blood from patients with IPF. The present study demonstrated that IL-10 expression in peripheral blood of patients with IPF is increased significantly compared with healthy subjects. Activation of the IL-10/IL-10R1 signaling pathway promoted the viability and collagen synthesis and secretion of pulmonary fibroblasts, leading to pulmonary fibrosis. The present study provided experimental basis for further understanding the development mechanism of pulmonary fibrosis.

摘要

间质性肺炎是一种由多种原因引起的肺间质炎症和纤维化疾病,可导致呼吸功能障碍并威胁患者生命。本研究旨在探讨白细胞介素(IL)-10在间质性肺炎患者外周血中的表达及其在肺成纤维细胞中的生物学功能。共纳入42例特发性肺纤维化(IPF)患者和20名健康受试者。采用酶联免疫吸附测定(ELISA)法测定患者和健康受试者血清中IL-10浓度。成功从肺组织中分离出原代成纤维细胞并通过形态学进行鉴定。采用细胞计数试剂盒(CCK-8)法测定IL-10表达对细胞活力的影响。采用蛋白质免疫印迹法测定Ⅰ型胶原蛋白α1(COL1a1)、Ⅰ型胶原蛋白α2(COL1a2)和IL-10受体1(IL-10R1)蛋白表达。采用流式细胞术进行细胞周期分析并测定IL-10阳性细胞数量。与健康受试者相比,IPF患者血清中IL-10表达更高。IL-10可促进人胚肺成纤维细胞(MRC-5细胞)和原代肺成纤维细胞的活力以及胶原蛋白的合成与分泌。IL-10和IL-10受体(R)1在MRC-5细胞的活力和胶原蛋白合成中发挥调节作用。IPF患者外周血中IL-10阳性表达的外周单个核淋巴细胞比例升高。本研究表明,与健康受试者相比,IPF患者外周血中IL-10表达显著增加。IL-10/IL-IO R1信号通路的激活促进了肺成纤维细胞的活力以及胶原蛋白的合成与分泌,导致肺纤维化。本研究为进一步了解肺纤维化的发病机制提供了实验依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32de/9257754/75396a4e6f23/etm-24-02-11445-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32de/9257754/d600aeb5609c/etm-24-02-11445-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32de/9257754/d2c7254b894f/etm-24-02-11445-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32de/9257754/9e643fa3fa59/etm-24-02-11445-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32de/9257754/75396a4e6f23/etm-24-02-11445-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32de/9257754/d600aeb5609c/etm-24-02-11445-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32de/9257754/d2c7254b894f/etm-24-02-11445-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32de/9257754/9e643fa3fa59/etm-24-02-11445-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32de/9257754/75396a4e6f23/etm-24-02-11445-g03.jpg

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