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Updated: Aug 17, 2026

Establishing a Silicosis Rat Model via Exposure of Whole-Body to Respirable Silica
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Establishing a Silicosis Rat Model via Exposure of Whole-Body to Respirable Silica

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Macrophage-derived exosomal HMGB3 regulates silica-induced pulmonary inflammation by promoting M1 macrophage

Xiaofeng Qin1, Zhiyuan Niu1, Hui Chen2

  • 1Department of Pathology, School of Basic Medical Science, Central South University, Changsha, China.

Particle and Fibre Toxicology
|March 8, 2024
PubMed
Abstract

Insights

Macrophage-derived exosomes carrying high mobility group box 3 (HMGB3) promote silica-induced lung inflammation. Exosomal HMGB3 activates key inflammatory pathways and recruits immune cells, highlighting its role in silicosis pathogenesis.

Area of Science:

  • Pulmonary immunology
  • Cellular and molecular biology
  • Exosome biology

Background:

  • Silicosis is characterized by chronic inflammation and fibrosis, with incompletely understood inflammatory mediators.
  • Macrophage-derived exosomes are known inflammatory modulators, but their specific role in silicosis remains unexplored.

Purpose of the Study:

  • To investigate the function of macrophage-derived exosomal high mobility group box 3 (HMGB3) in silica-induced pulmonary inflammation.

Main Methods:

  • Evaluated inflammatory response and monocyte/macrophage recruitment using immunofluorescence, flow cytometry, and Transwell assays.
  • Assessed inflammatory cytokine expression via RT-PCR and ELISA.
  • Analyzed signaling pathway activation using Western blot.

Main Results:

  • Silica-exposed macrophages released exosomes with increased HMGB3 expression.
  • Exosomal HMGB3 upregulated inflammatory cytokines and activated STAT3/MAPK/NF-κB pathways in monocytes/macrophages.
  • Exosomal HMGB3 promoted monocyte/macrophage migration via CCR2.

Conclusions:

  • Exosomal HMGB3 acts as a proinflammatory mediator in silica-induced inflammation.
  • It enhances the inflammatory response and immune cell recruitment by modulating STAT3/MAPK/NF-κB/CCR2 signaling pathways.
Keywords:
HMGB3InflammationMacrophage polarizationSilicosis

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