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Chapter 21 : Myeloid Cells in Cutaneous Wound Repair

Authors: Jenna L. Cash1, Paul Martin2
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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
Content Type: Monograph
Publication Year: 2017

Category: Microbial Genetics and Molecular Biology

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Myeloid Cells in Cutaneous Wound Repair, Page 1 of 2

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Abstract:

Wound repair is a complex and dynamic process that aims to restore cellular structures and tissue layers to damaged organs. Damage to the anatomical barriers against the environment, including the skin and gastrointestinal and respiratory systems, opens the organism to microbial invasion, and so the first function of the repair process is to temporarily seal this breach with a platelet plug and to counter infection as rapidly as possible. In skin wounds in healthy adults, barrier function is efficiently restored; however, repair of deeper dermal structures culminates in scar formation with loss of the original tissue structure and function. Tissue damage can be inflicted to a variety of organs by diverse stimuli, including ischemia (heart attack), burns (chemical, heat, or electrical), trauma, surgery, or infection. Although the anatomical sites injured may be distinct, for example, the immune-privileged cornea versus the gut with its complex microbiome, or the heart with its propensity for fibrosis, it is generally acknowledged that repair of all tissues shares basic commonalities. The wound-healing response can thus be typically divided into four overlapping phases: hemostasis, inflammation, cell migration/proliferation, and remodeling ( Fig. 1 ) ( ).

Citation: Cash J, Martin P. 2017. Myeloid Cells in Cutaneous Wound Repair, p 385-403. In Gordon S (ed), Myeloid Cells in Health and Disease. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.MCHD-0017-2015
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Myeloid Cells in Cutaneous Wound Repair
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Citation: Cash J, Martin P. 2017. Myeloid Cells in Cutaneous Wound Repair, p 385-403. In Gordon S (ed), Myeloid Cells in Health and Disease. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.MCHD-0017-2015
/content/10.1128/9781555819194.chap21.fig21-1
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.

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10.1128/9781555819194/fig21-1.gif
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.

Citation: Cash J, Martin P. 2017. Myeloid Cells in Cutaneous Wound Repair, p 385-403. In Gordon S (ed), Myeloid Cells in Health and Disease. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.MCHD-0017-2015
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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.

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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.

Citation: Cash J, Martin P. 2017. Myeloid Cells in Cutaneous Wound Repair, p 385-403. In Gordon S (ed), Myeloid Cells in Health and Disease. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.MCHD-0017-2015
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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.

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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.

Citation: Cash J, Martin P. 2017. Myeloid Cells in Cutaneous Wound Repair, p 385-403. In Gordon S (ed), Myeloid Cells in Health and Disease. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.MCHD-0017-2015
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