Attenuation of skin injury by a MARCO targeting PLGA nanoparticle

Abstract Cutaneous exposure to the DNA alkylating class of chemotherapeutic agents including nitrogen mustard (NM) leads to both skin injury and systemic inflammation. Circulating myeloid subsets recruited to the skin act to further exacerbate local tissue damage while interfering with the wound hea...

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Main Authors: Ummiye V. Onay, Dan Xu, Dauren Biyashev, Spencer T. Evans, Michael M. Demczuk, Tobias Neef, Joseph R. Podojil, Sara Beddow, Nathan C. Gianneschi, I. Caroline Le Poole, Stephen D. Miller, Kurt Q. Lu
Format: Article
Language:English
Published: Nature Portfolio 2024-12-01
Series:npj Regenerative Medicine
Online Access:https://doi.org/10.1038/s41536-024-00381-z
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author Ummiye V. Onay
Dan Xu
Dauren Biyashev
Spencer T. Evans
Michael M. Demczuk
Tobias Neef
Joseph R. Podojil
Sara Beddow
Nathan C. Gianneschi
I. Caroline Le Poole
Stephen D. Miller
Kurt Q. Lu
author_facet Ummiye V. Onay
Dan Xu
Dauren Biyashev
Spencer T. Evans
Michael M. Demczuk
Tobias Neef
Joseph R. Podojil
Sara Beddow
Nathan C. Gianneschi
I. Caroline Le Poole
Stephen D. Miller
Kurt Q. Lu
author_sort Ummiye V. Onay
collection DOAJ
description Abstract Cutaneous exposure to the DNA alkylating class of chemotherapeutic agents including nitrogen mustard (NM) leads to both skin injury and systemic inflammation. Circulating myeloid subsets recruited to the skin act to further exacerbate local tissue damage while interfering with the wound healing process. We demonstrate herein that intravenous delivery of poly(lactic-co-glycolic acid) immune-modifying nanoparticles (PLGA-IMPs) shortly after NM exposure restricts accumulation of macrophages and inflammatory monocytes at the injury site, resulting in attenuated skin pathology. Furthermore, PLGA-IMPs induce an early influx and local enrichment of Foxp3+ regulatory T cells (Treg) in the skin lesions critical for the suppression of myeloid cell-pro-inflammatory responses via induction of IL-10 and TGF-β in the cutaneous milieu. Functional depletion of CD4+ Tregs ablates the efficacy of PLGA-IMPs accompanied by a loss of local accumulation of anti-inflammatory cytokines essential for wound healing. Thus, in severe skin trauma, PLGA-IMPs may have therapeutic potential via modulation of inflammatory myeloid cells and regulatory T lymphocytes.
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spelling doaj-art-ee72089f6b5b4526b932dafa4b2f485a2025-08-20T02:30:56ZengNature Portfolionpj Regenerative Medicine2057-39952024-12-019111110.1038/s41536-024-00381-zAttenuation of skin injury by a MARCO targeting PLGA nanoparticleUmmiye V. Onay0Dan Xu1Dauren Biyashev2Spencer T. Evans3Michael M. Demczuk4Tobias Neef5Joseph R. Podojil6Sara Beddow7Nathan C. Gianneschi8I. Caroline Le Poole9Stephen D. Miller10Kurt Q. Lu11Department of Dermatology, Feinberg School of Medicine, Northwestern UniversityDepartment od Microbiology-Immunology, Feinberg School of Medicine, Northwestern UniversityDepartment of Dermatology, Feinberg School of Medicine, Northwestern UniversityDepartment of Dermatology, Feinberg School of Medicine, Northwestern UniversityDepartment of Dermatology, Feinberg School of Medicine, Northwestern UniversityDepartment od Microbiology-Immunology, Feinberg School of Medicine, Northwestern UniversityDepartment od Microbiology-Immunology, Feinberg School of Medicine, Northwestern UniversityDepartment od Microbiology-Immunology, Feinberg School of Medicine, Northwestern UniversityDepartment of Chemistry, Northwestern UniversityDepartment of Dermatology, Feinberg School of Medicine, Northwestern UniversityDepartment of Dermatology, Feinberg School of Medicine, Northwestern UniversityDepartment of Dermatology, Feinberg School of Medicine, Northwestern UniversityAbstract Cutaneous exposure to the DNA alkylating class of chemotherapeutic agents including nitrogen mustard (NM) leads to both skin injury and systemic inflammation. Circulating myeloid subsets recruited to the skin act to further exacerbate local tissue damage while interfering with the wound healing process. We demonstrate herein that intravenous delivery of poly(lactic-co-glycolic acid) immune-modifying nanoparticles (PLGA-IMPs) shortly after NM exposure restricts accumulation of macrophages and inflammatory monocytes at the injury site, resulting in attenuated skin pathology. Furthermore, PLGA-IMPs induce an early influx and local enrichment of Foxp3+ regulatory T cells (Treg) in the skin lesions critical for the suppression of myeloid cell-pro-inflammatory responses via induction of IL-10 and TGF-β in the cutaneous milieu. Functional depletion of CD4+ Tregs ablates the efficacy of PLGA-IMPs accompanied by a loss of local accumulation of anti-inflammatory cytokines essential for wound healing. Thus, in severe skin trauma, PLGA-IMPs may have therapeutic potential via modulation of inflammatory myeloid cells and regulatory T lymphocytes.https://doi.org/10.1038/s41536-024-00381-z
spellingShingle Ummiye V. Onay
Dan Xu
Dauren Biyashev
Spencer T. Evans
Michael M. Demczuk
Tobias Neef
Joseph R. Podojil
Sara Beddow
Nathan C. Gianneschi
I. Caroline Le Poole
Stephen D. Miller
Kurt Q. Lu
Attenuation of skin injury by a MARCO targeting PLGA nanoparticle
npj Regenerative Medicine
title Attenuation of skin injury by a MARCO targeting PLGA nanoparticle
title_full Attenuation of skin injury by a MARCO targeting PLGA nanoparticle
title_fullStr Attenuation of skin injury by a MARCO targeting PLGA nanoparticle
title_full_unstemmed Attenuation of skin injury by a MARCO targeting PLGA nanoparticle
title_short Attenuation of skin injury by a MARCO targeting PLGA nanoparticle
title_sort attenuation of skin injury by a marco targeting plga nanoparticle
url https://doi.org/10.1038/s41536-024-00381-z
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