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Updated: May 5, 2026
Establishing a Silicosis Rat Model via Exposure of Whole-Body to Respirable Silica
Published on: October 28, 2022
Effect of macrophage-to-myofibroblast transition on silicosis
Fei Geng1,2, Jingrou Xu1, Xichen Ren1
1Hebei Key Laboratory for Organ Fibrosis Research, School of Public Health, North China University of Science and Technology, Tangshan, China.
Background:
The aim was to explore the effect of macrophage polarization and macrophage-to-myofibroblast transition (MMT) in silicosis.
Methods:
Male Wistar rats were divided into a control group and a silicosis group developed using a HOPE MED 8050 dynamic automatic dusting system. Murine macrophage MH-S cells were randomly divided into a control group and an SiO2 group. The pathological changes in lung tissue were observed using hematoxylin and eosin (HE) and Van Gieson (VG) staining. The distribution and location of macrophage marker (F4/80), M1 macrophage marker (iNOS), M2 macrophage marker (CD206), and myofibroblast marker (α-smooth muscle actin [α-SMA]) were detected using immunohistochemical and immunofluorescent staining. The expression changes in iNOS, Arg, α-SMA, vimentin, and type I collagen (Col I) were measured using Western blot.
Results:
The results of HE and VG staining showed obvious silicon nodule formation and the distribution of thick collagen fibers in the lung tissue of the silicosis group. Macrophage marker F4/80 increased gradually from 8 to 32 weeks after exposure to silica. Immunohistochemical and immunofluorescent staining results revealed that there were more iNOS-positive cells and some CD206-positive cells in the lung tissue of the silicosis group at 8 weeks. More CD206-positive cells were found in the silicon nodules of the lung tissues in the silicosis group at 32 weeks. Western blot analysis showed that the expressions of Inducible nitric oxide synthase and Arg protein in the lung tissues of the silicosis group were upregulated compared with those of the control group. The results of immunofluorescence staining showed the co-expression of F4/80, α-SMA, and Col I, and CD206 and α-SMA were co-expressed in the lung tissue of the silicosis group. The extracted rat alveolar lavage fluid revealed F4/80+α-SMA+, CD206+α-SMA+, and F4/80+α-SMA+Col I+ cells using immunofluorescence staining. Similar results were also found in MH-S cells induced by SiO2.
Conclusions:
The development of silicosis is accompanied by macrophage polarization and MMT.
Insights
Silicosis development involves macrophage polarization and transition to myofibroblasts. This study observed these changes in rat lung tissue and cell models after silica exposure, confirming their role in the disease progression.
Area of Science:
- Pulmonary Pathology
- Cell Biology
- Immunology
Background:
- Silicosis is a serious lung disease caused by silica dust inhalation.
- The role of macrophage polarization and macrophage-to-myofibroblast transition (MMT) in silicosis pathogenesis requires further investigation.
Purpose of the Study:
- To investigate the effects of macrophage polarization and MMT in the development of silicosis.
- To analyze the cellular and molecular changes associated with silica exposure in lung tissue and macrophages.
Main Methods:
- Silicosis was induced in male Wistar rats using a dynamic automatic dusting system.
- Murine macrophage MH-S cells were exposed to SiO2.
- Pathological changes, macrophage markers (F4/80, iNOS, CD206), and myofibroblast markers (α-SMA) were assessed using HE, VG, immunohistochemical, and immunofluorescent staining.
- Protein expression of iNOS, Arg, α-SMA, vimentin, and Col I was measured by Western blot.
Main Results:
- Silicosis group exhibited silicon nodule formation and collagen deposition.
- Macrophage marker F4/80 expression increased over time post-silica exposure.
- Increased iNOS and CD206 positive cells were observed, with CD206 positive cells accumulating in silicon nodules at later stages.
- Upregulation of iNOS, Arg, α-SMA, and Col I was confirmed by Western blot.
- Co-expression of macrophage and myofibroblast markers (F4/80, CD206, α-SMA, Col I) was detected in lung tissue and alveolar lavage fluid, consistent with findings in SiO2-induced MH-S cells.
Conclusions:
- Silicosis development is characterized by significant macrophage polarization.
- Macrophage-to-myofibroblast transition (MMT) is a key process occurring during silicosis.
- These findings highlight the critical roles of macrophage polarization and MMT in the pathogenesis of silicosis.
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