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Updated: May 19, 2026
Adoptive Transfer of IL-33-Stimulated Macrophages into Bleomycin-Induced Mouse Models to Study Their Effect on Idiopathic Pulmonary Fibrosis In Vivo
Published on: May 5, 2023
Study on mannose-modified panax notoginseng polysaccharide self-assembled micelles to reduce idiopathic pulmonary
Bang-Yun Liu1, Ya-Ni Zhang2, Ge Zhang2
1School of Pharmacy, Liaoning University of Traditional Chinese Medicine, Dalian 116600, China; Shenyang Key Laboratory of Chinese Medicine targeted Delivery Key Laboratory, Shenyang 110148, China.
Abstract:
Idiopathic pulmonary fibrosis (IPF) is a life-threatening respiratory disease characterized by excessive proliferation of myofibroblasts and abnormal accumulation of extracellular matrix. At present, the treatment is limited. M2 macrophages play a key role in the pathogenesis of IPF. M2 macrophages are the main source of pro-fibrotic cytokine TGF-β1, which drives the progression of IPF by inducing epithelial-mesenchymal transition (EMT) and fibroblast-to-myofibroblast transition (FMT), and highly express mannose (Man) specific surface receptors. This feature provides an important target basis for us to design targeted drug delivery systems. Emodin (Emo) is a potential anti-fibrosis drug, but its poor water solubility and low bioavailability are limited in clinical practice. Therefore, we constructed a self-assembling M2-targeting micellar (Man-Sa-Pnp-Emo@Ms) to target M2-type macrophages and inhibit the secretion of TGF-β1, blocking the core pathological process of pulmonary fibrosis. Cellular uptake, cytotoxicity, and anti-fibrotic effects (inhibition of fibroblast proliferation, invasion, and metastasis) were evaluated in vitro, and their targeting and anti-fibrotic effects were verified by in vivo imaging and histological staining (HE, Masson, immunofluorescence). The results showed that Man-Sa-Pnp-Emo@Ms had a homogeneous spherical structure, which improved the solubility of Emo and reduced the release of M2-type macrophage-derived TGF-β1. It inhibited FMT transformation and extracellular matrix accumulation (ECM) and exerted anti-fibrotic effects without damaging tissue-resident macrophages in vitro and in a bleomycin-induced mouse model. This work provides a novel nanodelivery strategy for the precision treatment of idiopathic pulmonary fibrosis.
Insights
A novel nanoparticle effectively targets M2 macrophages, delivering emodin to treat idiopathic pulmonary fibrosis (IPF) by inhibiting TGF-β1 and reducing fibrosis. This strategy improves drug delivery and reduces disease progression.
Area of Science:
- Biomedical Engineering
- Nanotechnology
- Respiratory Medicine
Background:
- Idiopathic pulmonary fibrosis (IPF) is a severe lung disease with limited treatment options.
- M2 macrophages are key drivers of IPF pathogenesis, producing pro-fibrotic TGF-β1.
- Emodin shows anti-fibrotic potential but suffers from poor solubility and bioavailability.
Purpose of the Study:
- To develop a targeted drug delivery system for IPF treatment.
- To create M2 macrophage-targeting micelles loaded with emodin (Man-Sa-Pnp-Emo@Ms).
- To inhibit TGF-β1 secretion and block the core pathological processes of pulmonary fibrosis.
Main Methods:
- Constructed self-assembling M2-targeting micelles (Man-Sa-Pnp-Emo@Ms).
- Evaluated cellular uptake, cytotoxicity, and anti-fibrotic effects in vitro.
- Verified targeting and anti-fibrotic efficacy in vivo using imaging and histological analysis in a bleomycin-induced mouse model.
Main Results:
- Man-Sa-Pnp-Emo@Ms exhibited a homogeneous spherical structure, enhancing emodin solubility.
- The micelles effectively reduced M2 macrophage-derived TGF-β1 secretion.
- In vitro and in vivo studies demonstrated inhibition of fibroblast-to-myofibroblast transition (FMT), extracellular matrix accumulation, and anti-fibrotic effects without harming tissue macrophages.
Conclusions:
- Man-Sa-Pnp-Emo@Ms represents a novel nanodelivery strategy for IPF precision treatment.
- Targeting M2 macrophages with emodin-loaded micelles effectively inhibits pulmonary fibrosis progression.
- This approach offers a promising therapeutic avenue for idiopathic pulmonary fibrosis.