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

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.