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Myeloid Cells in Cutaneous Wound Repair

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  • Authors: Jenna L. Cash1, Paul Martin2
  • Editor: Siamon Gordon3
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: MRC Centre for Inflammation Research, The University of Edinburgh, The Queen’s Medical Research Institute, Edinburgh, EH16 4TJ; 2: School of Biochemistry, Medical Sciences, University Walk, Bristol University, Bristol BS8 1TD, United Kingdom; 3: Oxford University, Oxford, United Kingdom
  • Source: microbiolspec June 2016 vol. 4 no. 3 doi:10.1128/microbiolspec.MCHD-0017-2015
  • Received 11 August 2015 Accepted 01 September 2015 Published 03 June 2016
  • Jenna L. Cash, jenna.cash@ed.ac.uk; Paul Martin, paul.martin@bristol.ac.uk
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  • Abstract:

    Cutaneous wound repair is a complex, dynamic process with the goal of rapidly sealing any breach in the skin’s protective barrier. Myeloid cells compose a significant proportion of the inflammatory cells recruited to a wound site and play important roles in decontaminating the injured tissue of any invading microorganisms. Subsequently, myeloid cells are able to influence many aspects of the healing response, in part through their capacity to release a large array of signaling molecules that allow them to communicate with and regulate the behavior of other wound cells and in turn, be themselves exquisitely regulated by the wound microenvironment. Macrophages, for example, appear to play important, temporally changing roles in the initiation of scarring and subsequently in matrix remodeling to resolve fibrosis. In this way, myeloid cells seem to play both positive (e.g., pathogen killing and matrix remodeling) and negative (e.g., scarring) roles in wound repair. Further research is of course needed to elucidate the precise temporal and spatial myeloid cell phenotypes and behaviors and ultimately to design effective strategies to optimize the beneficial functions of these cells while minimizing their detrimental contributions to improve wound healing in the clinic.

  • Citation: Cash J, Martin P. 2016. Myeloid Cells in Cutaneous Wound Repair. Microbiol Spectrum 4(3):MCHD-0017-2015. doi:10.1128/microbiolspec.MCHD-0017-2015.

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/content/journal/microbiolspec/10.1128/microbiolspec.MCHD-0017-2015
2016-06-03
2017-07-25

Abstract:

Cutaneous wound repair is a complex, dynamic process with the goal of rapidly sealing any breach in the skin’s protective barrier. Myeloid cells compose a significant proportion of the inflammatory cells recruited to a wound site and play important roles in decontaminating the injured tissue of any invading microorganisms. Subsequently, myeloid cells are able to influence many aspects of the healing response, in part through their capacity to release a large array of signaling molecules that allow them to communicate with and regulate the behavior of other wound cells and in turn, be themselves exquisitely regulated by the wound microenvironment. Macrophages, for example, appear to play important, temporally changing roles in the initiation of scarring and subsequently in matrix remodeling to resolve fibrosis. In this way, myeloid cells seem to play both positive (e.g., pathogen killing and matrix remodeling) and negative (e.g., scarring) roles in wound repair. Further research is of course needed to elucidate the precise temporal and spatial myeloid cell phenotypes and behaviors and ultimately to design effective strategies to optimize the beneficial functions of these cells while minimizing their detrimental contributions to improve wound healing in the clinic.

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Figures

Image of FIGURE 1
FIGURE 1

Time course of the cutaneous wound repair response. (Top) The time relationship between different wound repair processes and the cells involved. Wound repair is often thought of as occurring in four phases: hemostasis (platelet-mediated blood coagulation and immediate damage-signaling events), inflammation (leukocyte recruitment to the site of injury), migration and proliferation (keratinocyte proliferation and migration to reepithelialize the wound, fibroblast migration, contraction, and collagen deposition leading to scar formation), and remodeling (resolution of wound vessels and remodeling of the scar tissue). (Bottom) Representative hematoxylin and eosin-stained wound midsections from days 1, 4, 7, and 14 after excisional wounding are shown. These depict important features of each stage of repair, including scab formation and loss, inflammatory cell influx, and reepithelialization.

Source: microbiolspec June 2016 vol. 4 no. 3 doi:10.1128/microbiolspec.MCHD-0017-2015
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Image of FIGURE 2
FIGURE 2

Myeloid cells in wounds. Diagram depicting myeloid cells involved in cutaneous repair along with some of the key receptors with which they sense wound signals, and signaling molecules and enzymes released in response to the specific signals that these cells process. Key receptors shared by these cells are noted in the central green box, while neutrophil, mast cell, and eosinophil granules are shown as purple or pink filled circles. Cells are not drawn to scale. Abbreviations: LFA, lymphocyte function-associated antigen; MCP, monocyte chemoattractant protein; PRR, pattern recognition receptor.

Source: microbiolspec June 2016 vol. 4 no. 3 doi:10.1128/microbiolspec.MCHD-0017-2015
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Image of FIGURE 3
FIGURE 3

Acute versus chronic wound healing. A healthy repairing acute wound is protected by a scab throughout much of the healing response. During this period, the various missing tissue layers are replaced by cell migration and proliferation, and this is supported by an influx of myeloid cells, which subsequently resolve after the wound has healed. In a chronic wound, a scab may not be present but a bacterial biofilm invariably is, and certain cells migrate poorly. There is a prolonged and elevated influx of myeloid cells, with the inflammatory response overflowing into the adjacent tissue and often extending into the underlying muscle or bone.

Source: microbiolspec June 2016 vol. 4 no. 3 doi:10.1128/microbiolspec.MCHD-0017-2015
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