“Immunomodulatory nanoparticles elicit antifibrotic monocyte activation to resolve murine pulmonary fibrosis”

Organ fibrosis can follow from tissue injury and substantially impairs organ function, but it is incurable and has limited therapeutic options. Myeloid immune cells drive fibrosis onset and progression, but they can also mediate fibrosis resolution. We used polymeric NPs made from clinically translatable biomaterials to harness the antifibrotic capacity of immune cells as a fibrosis therapy. We found that intravenous NPs can reprogram myeloid cells to acquire an antifibrotic phenotype in a mouse model of pulmonary fibrosis. NPs increased myeloid activation and pulmonary recruitment while decreasing fibrosis, showing that directed immune activation, instead of suppression, could be an effective therapeutic strategy for fibrosis.

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Publication Details

Journal
bioRxiv (Cold Spring Harbor Laboratory)
Published
2025-12-24
DOI
https://doi.org/10.64898/2025.12.22.696047
Primary Topic
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
Type
article
Field-Weighted Citation Impact
0.00
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article

“Immunomodulatory nanoparticles elicit antifibrotic monocyte activation to resolve murine pulmonary fibrosis”

Francina Gonzalez De Los Santos, Hannah Viola, Rita Medina Costa, Ryan Chen et al.
bioRxiv (Cold Spring Harbor Laboratory)
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
article

“Immunomodulatory nanoparticles elicit antifibrotic monocyte activation to resolve murine pulmonary fibrosis”

Francina Gonzalez De Los Santos, Hannah Viola, Rita Medina Costa, Ryan Chen, Hannah Carter, Zharia Hunter, Riley McDonald, Kate Griffin, Lonnie Shea, Brennan Callow, Marisa Martinez
article en

Abstract

Organ fibrosis can follow from tissue injury and substantially impairs organ function, but it is incurable and has limited therapeutic options. Myeloid immune cells drive fibrosis onset and progression, but they can also mediate fibrosis resolution. We used polymeric NPs made from clinically translatable biomaterials to harness the antifibrotic capacity of immune cells as a fibrosis therapy. We found that intravenous NPs can reprogram myeloid cells to acquire an antifibrotic phenotype in a mouse model of pulmonary fibrosis. NPs increased myeloid activation and pulmonary recruitment while decreasing fibrosis, showing that directed immune activation, instead of suppression, could be an effective therapeutic strategy for fibrosis.

bioRxiv (Cold Spring Harbor Laboratory)
University of Michigan (US)
Good health and well-being
Openalex Percentile: Top 28%
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
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“Immunomodulatory nanoparticles elicit antifibrotic monocyte activation to resolve murine pulmonary fibrosis” — Francina Gonzalez De Los Santos, Hannah Viola, et al. · bioRxiv (Cold Spring Harbor Laboratory) (2025) | TGRS Research Map | TGRS