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结节病外泌体刺激单核细胞产生促炎细胞因子和 CCL2。

Sarcoidosis exosomes stimulate monocytes to produce pro-inflammatory cytokines and CCL2.

机构信息

Division of Immunology and Allergy, Department of Medicine Solna, Karolinska Institutet, Solna, Sweden.

Department of Clinical Immunology and Transfusion Medicine, Karolinska University Hospital, Solna, Sweden.

出版信息

Sci Rep. 2020 Sep 18;10(1):15328. doi: 10.1038/s41598-020-72067-7.

Abstract

Pulmonary sarcoidosis has unknown etiology, a difficult diagnostic procedure and no curative treatment. Extracellular vesicles including exosomes are nano-sized entities released from all cell types. Previous studies of exosomes from bronchoalveolar lavage fluid (BALF) of sarcoidosis patients have revealed pro-inflammatory components and abilities, but cell sources and mechanisms have not been identified. In the current study, we found that BALF exosomes from sarcoidosis patients, but not from healthy individuals, induced a dose-dependent elevation of intracellular IL-1β in monocytes. Analyses of supernatants showed that patient exosomes also induced release of IL-1β, IL-6 and TNF from both PBMCs and enriched monocytes, suggesting that the observed effect is direct on monocytes. The potently chemotactic chemokine CCL2 was induced by exosomes from a subgroup of patients, and in a blocking assay the exosome-induced CCL2 was reduced for 13 out of 19 patients by the asthma drug Montelukast, a cysteinyl leukotriene receptor antagonist. Further, reactive oxygen species generation by PBMCs was induced to a higher degree by patient exosomes compared to healthy exosomes. These findings add to an emerging picture of exosomes as mediators and disseminators of inflammation, and open for further investigations of the link between CCL2 and exosomal leukotrienes in sarcoidosis.

摘要

肺结节病的病因不明,诊断程序复杂,且无治愈方法。细胞外囊泡(包括外泌体)是所有细胞类型释放的纳米级实体。先前对结节病患者支气管肺泡灌洗液(BALF)中的外泌体的研究揭示了促炎成分和能力,但细胞来源和机制尚未确定。在本研究中,我们发现结节病患者的 BALF 外泌体而非健康个体的 BALF 外泌体可诱导单核细胞内的 IL-1β 呈剂量依赖性升高。对上清液的分析表明,患者的外泌体还可诱导 PBMC 和富集的单核细胞释放 IL-1β、IL-6 和 TNF,表明观察到的效应是直接作用于单核细胞。一组患者的外泌体诱导了趋化因子 CCL2 的强烈趋化作用,在阻断试验中,哮喘药物孟鲁司特(一种半胱氨酰白三烯受体拮抗剂)可使 19 名患者中的 13 名患者的外泌体诱导的 CCL2 减少。此外,与健康的外泌体相比,患者的外泌体更能诱导 PBMC 产生更多的活性氧物质。这些发现进一步证明了外泌体作为炎症的介质和传播者的作用,并为进一步研究结节病中 CCL2 和外泌体白三烯之间的联系开辟了道路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02b2/7501276/50e3726abb9a/41598_2020_72067_Fig1_HTML.jpg

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