Non-classical monocytes are biased progenitors of wound healing macrophages during soft tissue injury

Abstract Successful tissue repair requires the activities of myeloid cells such as monocytes and macrophages that guide the progression of inflammation and healing outcome. Immunoregenerative materials leverage the function of endogenous immune cells to orchestrate complex mechanisms of repair; howe...

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Autores principales: Claire E. Olingy, Cheryl L. San Emeterio, Molly E. Ogle, Jack R. Krieger, Anthony C. Bruce, David D. Pfau, Brett T. Jordan, Shayn M. Peirce, Edward A. Botchwey
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Publicado: Nature Portfolio 2017
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Acceso en línea:https://doaj.org/article/97d46e2fdbb240baa119d3313447e572
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spelling oai:doaj.org-article:97d46e2fdbb240baa119d3313447e5722021-12-02T12:32:45ZNon-classical monocytes are biased progenitors of wound healing macrophages during soft tissue injury10.1038/s41598-017-00477-12045-2322https://doaj.org/article/97d46e2fdbb240baa119d3313447e5722017-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-00477-1https://doaj.org/toc/2045-2322Abstract Successful tissue repair requires the activities of myeloid cells such as monocytes and macrophages that guide the progression of inflammation and healing outcome. Immunoregenerative materials leverage the function of endogenous immune cells to orchestrate complex mechanisms of repair; however, a deeper understanding of innate immune cell function in inflamed tissues and their subsequent interactions with implanted materials is necessary to guide the design of these materials. Blood monocytes exist in two primary subpopulations, characterized as classical inflammatory or non-classical. While classical monocytes extravasate into inflamed tissue and give rise to macrophages or dendritic cells, the recruitment kinetics and functional role of non-classical monocytes remains unclear. Here, we demonstrate that circulating non-classical monocytes are directly recruited to polymer films within skin injuries, where they home to a perivascular niche and generate alternatively activated, wound healing macrophages. Selective labeling of blood monocyte subsets indicates that non-classical monocytes are biased progenitors of alternatively activated macrophages. On-site delivery of the immunomodulatory small molecule FTY720 recruits S1PR3-expressing non-classical monocytes that support vascular remodeling after injury. These results elucidate a previously unknown role for blood-derived non-classical monocytes as contributors to alternatively activated macrophages, highlighting them as key regulators of inflammatory response and regenerative outcome.Claire E. OlingyCheryl L. San EmeterioMolly E. OgleJack R. KriegerAnthony C. BruceDavid D. PfauBrett T. JordanShayn M. PeirceEdward A. BotchweyNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-16 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Claire E. Olingy
Cheryl L. San Emeterio
Molly E. Ogle
Jack R. Krieger
Anthony C. Bruce
David D. Pfau
Brett T. Jordan
Shayn M. Peirce
Edward A. Botchwey
Non-classical monocytes are biased progenitors of wound healing macrophages during soft tissue injury
description Abstract Successful tissue repair requires the activities of myeloid cells such as monocytes and macrophages that guide the progression of inflammation and healing outcome. Immunoregenerative materials leverage the function of endogenous immune cells to orchestrate complex mechanisms of repair; however, a deeper understanding of innate immune cell function in inflamed tissues and their subsequent interactions with implanted materials is necessary to guide the design of these materials. Blood monocytes exist in two primary subpopulations, characterized as classical inflammatory or non-classical. While classical monocytes extravasate into inflamed tissue and give rise to macrophages or dendritic cells, the recruitment kinetics and functional role of non-classical monocytes remains unclear. Here, we demonstrate that circulating non-classical monocytes are directly recruited to polymer films within skin injuries, where they home to a perivascular niche and generate alternatively activated, wound healing macrophages. Selective labeling of blood monocyte subsets indicates that non-classical monocytes are biased progenitors of alternatively activated macrophages. On-site delivery of the immunomodulatory small molecule FTY720 recruits S1PR3-expressing non-classical monocytes that support vascular remodeling after injury. These results elucidate a previously unknown role for blood-derived non-classical monocytes as contributors to alternatively activated macrophages, highlighting them as key regulators of inflammatory response and regenerative outcome.
format article
author Claire E. Olingy
Cheryl L. San Emeterio
Molly E. Ogle
Jack R. Krieger
Anthony C. Bruce
David D. Pfau
Brett T. Jordan
Shayn M. Peirce
Edward A. Botchwey
author_facet Claire E. Olingy
Cheryl L. San Emeterio
Molly E. Ogle
Jack R. Krieger
Anthony C. Bruce
David D. Pfau
Brett T. Jordan
Shayn M. Peirce
Edward A. Botchwey
author_sort Claire E. Olingy
title Non-classical monocytes are biased progenitors of wound healing macrophages during soft tissue injury
title_short Non-classical monocytes are biased progenitors of wound healing macrophages during soft tissue injury
title_full Non-classical monocytes are biased progenitors of wound healing macrophages during soft tissue injury
title_fullStr Non-classical monocytes are biased progenitors of wound healing macrophages during soft tissue injury
title_full_unstemmed Non-classical monocytes are biased progenitors of wound healing macrophages during soft tissue injury
title_sort non-classical monocytes are biased progenitors of wound healing macrophages during soft tissue injury
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/97d46e2fdbb240baa119d3313447e572
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