Role of CD163 in the mechanism of hydrophilic silica nanoparticle-induced pulmonary fibrosis

IF 2.7 3区医学 Q3 TOXICOLOGY

Toxicology in Vitro Pub Date : 2026-05-01 Epub Date: 2026-01-24 DOI:10.1016/j.tiv.2026.106201

Chaoya Ma, Yaotang Deng, Xiao Zhang, Qifeng Wu, Fengrong Lu, Jin Wu, Ying Zhang, Cuiju Wen

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引用次数: 0

Abstract

Objective

Silicosis, a progressive pulmonary fibrosis caused by silica dust exposure, remains a global occupational health threat, particularly with the rising use of nano-silica (nano-SiO₂) in industries. This study aims to explore the role of CD163 in pulmonary fibrosis induced by nano-silica (nano-SiO₂), and to evaluate its potential as a diagnostic biomarker by combining clinical analysis of patients with silicosis and in vitro validation models.

Method

Gene expression in BALF from stage I silicosis patients was analyzed by PCR. In vitro, THP-1-derived macrophages and MRC-5 fibroblasts were exposed to 100 μg/mL nano-SiO₂ (LC₅₀) in mono- and co-culture systems. CD163, CD68, and TNF-α levels were quantified via ELISA and Western blot.

Result

In patients, M2 markers (CD163/CD68) were upregulated, while M1 gene (TNF) was downregulated. In vitro, nano-SiO₂ increased macrophage CD163 by 1.7 times (P < 0.05) and decreased TNF-α by 42%. Co-culture further increased CD163 by 2.1 times (P < 0.01), indicating amplified M2 polarization via crosstalk.

Conclusion

Nano-SiO₂ drives M2 polarization (CD163↑/TNF-α↓). This finding suggests that CD163 may become one of the potential biomarkers for assessing the risk of pulmonary fibrosis induced by nano-SiO₂, providing important clues for the early warning and mechanism research of silicosis.

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CD163在亲水二氧化硅纳米颗粒诱导肺纤维化机制中的作用。

目的：矽肺病是一种由二氧化硅粉尘暴露引起的进行性肺纤维化，仍然是全球职业健康威胁，特别是随着纳米二氧化硅（纳米二氧化硅）在工业中的使用不断增加。本研究旨在通过对矽肺患者的临床分析和体外验证模型，探讨CD163在纳米二氧化硅（nano-SiO₂）诱导的肺纤维化中的作用，并评估其作为诊断性生物标志物的潜力。方法：采用PCR方法对ⅰ期矽肺患者BALF基因表达进行分析。在体外，thp -1来源的巨噬细胞和MRC-5成纤维细胞在单培养和共培养系统中暴露于100 μg/mL纳米sio₂（LC50）中。ELISA和Western blot检测各组小鼠CD163、CD68、TNF-α水平。结果：在患者中，M2标记物（CD163/CD68）上调，M1基因（TNF）下调。在体外，纳米sio₂使巨噬细胞CD163增加1.7倍(P 结论：纳米sio₂驱动M2极化（CD163↑/TNF-α↓）。这一发现提示CD163可能成为评估纳米sio2诱导肺纤维化风险的潜在生物标志物之一，为矽肺早期预警和机制研究提供重要线索。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Toxicology in Vitro 医学-毒理学

CiteScore

6.50

自引率

3.10%

发文量

181

审稿时长

65 days

期刊介绍： Toxicology in Vitro publishes original research papers and reviews on the application and use of in vitro systems for assessing or predicting the toxic effects of chemicals and elucidating their mechanisms of action. These in vitro techniques include utilizing cell or tissue cultures, isolated cells, tissue slices, subcellular fractions, transgenic cell cultures, and cells from transgenic organisms, as well as in silico modelling. The Journal will focus on investigations that involve the development and validation of new in vitro methods, e.g. for prediction of toxic effects based on traditional and in silico modelling; on the use of methods in high-throughput toxicology and pharmacology; elucidation of mechanisms of toxic action; the application of genomics, transcriptomics and proteomics in toxicology, as well as on comparative studies that characterise the relationship between in vitro and in vivo findings. The Journal strongly encourages the submission of manuscripts that focus on the development of in vitro methods, their practical applications and regulatory use (e.g. in the areas of food components cosmetics, pharmaceuticals, pesticides, and industrial chemicals). Toxicology in Vitro discourages papers that record reporting on toxicological effects from materials, such as plant extracts or herbal medicines, that have not been chemically characterized.