Evidence map›Paper›PMID 42372506›Full record

ArticleBiomaterials2026

Antifibrotic monocyte activation by nanoparticles resolves murine pulmonary fibrosis.

Hannah Viola, Hannah Carter, Kate Griffin, Rita Medina Costa, Riley McDonald, Brennan Callow, Francina Gonzalez de Los Santos, Peyton Panovich, Sean Carey, Marisa Martinez and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biomaterials, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors.

Hannah ViolaDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, 48109, USA; Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI, 48109, USA.
Hannah CarterDepartment of Microbiology and Immunology, University of Michigan, Ann Arbor, MI, 48109, USA.
Kate GriffinDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, 48109, USA.
Rita Medina CostaDepartment of Microbiology and Immunology, University of Michigan, Ann Arbor, MI, 48109, USA.
Riley McDonaldDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, 48109, USA; Department of Radiology, University of Michigan Medical School, Ann Arbor, MI, 48105, USA.
Brennan CallowDepartment of Radiology, University of Michigan Medical School, Ann Arbor, MI, 48105, USA.
Francina Gonzalez de Los SantosDepartment of Microbiology and Immunology, University of Michigan, Ann Arbor, MI, 48109, USA; Department of Internal Medicine - Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, MI, 48105, USA.
Peyton PanovichDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, 48109, USA.
Sean CareyDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, 48109, USA.
Marisa MartinezDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, 48109, USA.
Ryan ChenDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, 48109, USA.
Zharia HunterDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, 48109, USA.
Alexandra Piotrowski-DaspitDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, 48109, USA; Department of Internal Medicine - Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, MI, 48105, USA.
Gary LukerDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, 48109, USA; Department of Radiology, University of Michigan Medical School, Ann Arbor, MI, 48105, USA; Biointerfaces Institute, University of Michigan, 48109, Ann Arbor, MI, 48109, USA.
Bethany B MooreDepartment of Microbiology and Immunology, University of Michigan, Ann Arbor, MI, 48109, USA; Department of Internal Medicine - Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, MI, 48105, USA. Electronic address: bmoore@umich.edu.
Lonnie SheaDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, 48109, USA; Biointerfaces Institute, University of Michigan, 48109, Ann Arbor, MI, 48109, USA; Department of Chemical Engineering, University of Michigan, Ann Arbor, MI, 48109, USA. Electronic address: ldshea@umich.edu.

Funding

PULMONARY CELLULAR AND MOLECULAR BIOLOGY TRAININGT32HL007749 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Robert Pickett Dickson · 1993 to 2026
$19.9M
Nanoparticle-mediated reprogramming of circulating monocytes and neutrophils to decrease inflammation-mediated damage after traumaR01AI148076 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ANDERSON, AILEEN J, SHEA, LONNIE D · 2019 to 2023
$3.4M
Immune crosstalk in lung injury and fibrosisR35HL176572 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Bethany B. Moore · 2025 to 2026
$2.1M
Nanoparticles to reprogram innate immune cells and disrupt the metastatic nicheR01EB036030 · NIBIB · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI JACQUELINE SARA JERUSS, Lonnie D Shea · 2024 to 2026
$1.5M
The Role of Tryptophan Metabolism in Pulmonary FibrosisF30HL172413 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Hannah Carter · 2025 to 2026
$104k
NHLBI NIH HHS F30 HL172413NHLBI NIH HHS R35 HL176572NHLBI NIH HHS T32 HL007749NIAID NIH HHS R01 AI148076NIBIB NIH HHS R01 EB036030
6 · The paper itself

Abstract

Organ fibrosis presents a substantial disease burden with few therapeutic options. Innate immunity mediates fibrinogenesis, but also plays a major role in fibrinolysis. Here, we show that immunomodulatory nanoparticles (NPs) can harness this endogenous antifibrotic capacity by catalyzing monocyte activation leading to resolution of bleomycin-induced pulmonary fibrosis in vivo. Cargo-free NPs comprised of the degradable biopolymer poly(lactide-co-glycolide) (PLG) induce a transcriptional shift toward antifibrotic immune activation in profibrotic M2 macrophages (MΦs) in vitro. NPs stimulate M2 MΦs toward a glycolytic, rather than fatty acid oxidative, metabolism; suppress canonical M2 markers like arginase-1 (Arg1) and periostin ( ); and upregulate collagenases, hyaluronidases and immunoregulatory factors. When delivered intravenously in vivo, NPs resolve established bleomycin-induced pulmonary fibrosis and invert the trajectory of over 1000 genes from pre- to post-treatment according to bulk RNA-sequencing. NPs also suppress profibrotic signaling and increase expression of repair-associated pathways like peroxisome proliferator-activated receptor gamma (PPAR-γ), nuclear retinoic acid receptor (RAR), vascular endothelial growth factor (VEGF), and sphingolipid signaling in fibrotic lungs. Flow cytometry confirms that NPs induce monocyte recruitment to fibrotic lungs via enhanced integrin expression. Altogether, NPs induce a robust pro-regenerative signature comprised of ECM degradation, inflammation resolution, and tissue repair pathways, concomitant with increased NP+ monocyte recruitment to fibrotic lungs. This work demonstrates that monocytes are not intrinsically profibrotic, but rather, their effects are context-dependent, and they retain a capacity for fibrotic resolution under conditions that can be induced by materials with translational potential.

Indexed as

MonocytesNanoparticlesPulmonary FibrosisAnimalsBleomycinMacrophagesMaleMiceMice, Inbred C57BLBleomycinFibrosisImmunoengineeringImmunomodulationInflammationNanoparticles

Identifiers

PMID42372506
PMCPMC13524071

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.