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Related Experiment Video

Updated: Jun 30, 2026

Polyethyleneimine-coated Iron Oxide Nanoparticles as a Vehicle for the Delivery of Small Interfering RNA to Macrophages In Vitro and In Vivo

Polyethyleneimine-coated Iron Oxide Nanoparticles as a Vehicle for the Delivery of Small Interfering RNA to Macrophages In Vitro and In Vivo

Published on: February 5, 2019

Targeted RNA Therapy Reprograms Fibrotic Macrophages to Reverse Pulmonary Fibrosis.

Zhimin Song^1,2, Jingjing Chen^1,2, Jiaying Fan^1,2

¹State Key Laboratory of Respiratory Disease, the First Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 510120, China.

|June 29, 2026

Summary

This summary is machine-generated.

Targeted RNA therapy can reprogram profibrotic macrophages to combat pulmonary fibrosis. This approach remodels immune cell states, offering a new strategy for treating fibrotic lung diseases.

Keywords:

RNA therapeutics arginase-1 immunometabolism macrophage reprogramming pulmonary fibrosis

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Adoptive Transfer of IL-33-Stimulated Macrophages into Bleomycin-Induced Mouse Models to Study Their Effect on Idiopathic Pulmonary Fibrosis In Vivo

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

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Last Updated: Jun 30, 2026

Polyethyleneimine-coated Iron Oxide Nanoparticles as a Vehicle for the Delivery of Small Interfering RNA to Macrophages In Vitro and In Vivo

Polyethyleneimine-coated Iron Oxide Nanoparticles as a Vehicle for the Delivery of Small Interfering RNA to Macrophages In Vitro and In Vivo

Published on: February 5, 2019

Adoptive Transfer of IL-33-Stimulated Macrophages into Bleomycin-Induced Mouse Models to Study Their Effect on Idiopathic Pulmonary Fibrosis In Vivo

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

Area of Science:

Immunology
Molecular Biology
Pulmonary Medicine

Background:

Pulmonary fibrosis involves immune cells, particularly macrophages, that promote scarring.
Maladaptive immune responses reinforce fibroblast activation, driving disease progression.

Purpose of the Study:

To investigate if profibrotic macrophage states can be therapeutically remodeled using RNA-based modulation.
To explore targeted RNA delivery to alter macrophage regulatory circuitry and alleviate lung fibrosis.

Main Methods:

Single-cell transcriptomic and metabolomic analyses identified key regulatory programs in profibrotic macrophages.
A mannose-functionalized lipid nanoparticle platform was developed for targeted in vivo RNA delivery to CD206⁺ macrophages.
Therapeutic efficacy was assessed via Arginase-1 (Arg1) silencing and Interferon regulatory factor 5 (Irf5) mRNA delivery.

Main Results:

An Arg1-centered metabolic module was found to stabilize profibrotic macrophage states.
Targeted RNA delivery selectively reached CD206⁺ macrophages.
Arg1 silencing disrupted profibrotic pathways, while Irf5 mRNA shifted macrophages to an anti-fibrotic state, reducing pulmonary fibrosis.

Conclusions:

Macrophage states in pulmonary fibrosis can be therapeutically remodeled using targeted RNA modulation.
State-level immune reprogramming presents a potentially generalizable strategy for fibrotic diseases.