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  1. Article ; Online: Wound macrophages as key regulators of repair: origin, phenotype, and function.

    Brancato, Samielle K / Albina, Jorge E

    The American journal of pathology

    2010  Volume 178, Issue 1, Page(s) 19–25

    Abstract: Recent results call for the reexamination of the phenotype of wound macrophages and their role in tissue repair. These results include the characterization of distinct circulating monocyte populations with temporally restricted capacities to migrate into ...

    Abstract Recent results call for the reexamination of the phenotype of wound macrophages and their role in tissue repair. These results include the characterization of distinct circulating monocyte populations with temporally restricted capacities to migrate into wounds and the observation that the phenotype of macrophages isolated from murine wounds partially reflects those of their precursor monocytes, changes with time, and does not conform to current macrophage classifications. Moreover, findings in genetically modified mice lacking macrophages have confirmed that these cells are essential to normal wound healing because their depletion results in retarded and abnormal repair. This mini-review focuses on current knowledge of the phenotype of wound macrophages, their origin and fate, and the specific macrophage functions that underlie their reparative role in injured tissues, including the regulation of the cellular infiltration of the wound and the production of transforming growth factor-β and vascular endothelial growth factor.
    MeSH term(s) Animals ; Fibrosis ; Humans ; Macrophages/physiology ; Mice ; Neovascularization, Physiologic ; Neutrophils/physiology ; Transforming Growth Factor beta/physiology ; Vascular Endothelial Growth Factor A/physiology ; Wound Healing/physiology ; Wounds and Injuries/pathology ; Wounds and Injuries/physiopathology
    Chemical Substances Transforming Growth Factor beta ; Vascular Endothelial Growth Factor A
    Language English
    Publishing date 2010-12-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2943-9
    ISSN 1525-2191 ; 0002-9440
    ISSN (online) 1525-2191
    ISSN 0002-9440
    DOI 10.1016/j.ajpath.2010.08.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The monocyte to macrophage transition in the murine sterile wound.

    Meredith J Crane / Jean M Daley / Olivier van Houtte / Samielle K Brancato / William L Henry / Jorge E Albina

    PLoS ONE, Vol 9, Iss 1, p e

    2014  Volume 86660

    Abstract: The origin of wound repair macrophages is incompletely defined and was examined here in sterile wounds using the subcutaneous polyvinyl alcohol sponge implantation model in mice. Phenotypic analysis identified F4/80(+)Ly6C(hi)CD64(+)MerTK(-) monocytes ... ...

    Abstract The origin of wound repair macrophages is incompletely defined and was examined here in sterile wounds using the subcutaneous polyvinyl alcohol sponge implantation model in mice. Phenotypic analysis identified F4/80(+)Ly6C(hi)CD64(+)MerTK(-) monocytes and F4/80(+)Ly6C(low)CD64(+)MerTK(+) macrophages in the wound. Circulating monocytes were the precursors of inflammatory Ly6C(hi) wound monocytes. Ly6C(low)MerTK(+) macrophages appeared later, expressed CD206, CD11c, and MHC class II, produced cytokines consistent with repair function, and lacked a gene expression profile compatible with mesenchymal transition or fibroblastic transdifferentiation. Data also demonstrated that Ly6C(hi) wound cells were precursors of Ly6C(low) macrophages, although monocytes did not undergo rapid maturation but rather persisted in the wound as Ly6C(hi)MerTK(-) cells. MerTK-deficient mice were examined to determine whether MerTK-dependent signals from apoptotic cells regulated the maturation of wound macrophages. MerTK-deficient mice had day 14 cell compositions that resembled more immature wounds, with a smaller proportion of F4/80(+) cells and higher frequencies of Ly6G(+) neutrophils and Ly6C(hi) monocytes. The cytokine profile and number of apoptotic cells in day 14 wounds of MerTK-deficient mice was unaffected despite the alterations in cell composition. Overall, these studies identified a differentiation pathway in response to sterile inflammation in which monocytes recruited from the circulation acquire proinflammatory function, persist in the wound, and mature into repair macrophages.
    Keywords Medicine ; R ; Science ; Q
    Subject code 610
    Language English
    Publishing date 2014-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: The monocyte to macrophage transition in the murine sterile wound.

    Crane, Meredith J / Daley, Jean M / van Houtte, Olivier / Brancato, Samielle K / Henry, William L / Albina, Jorge E

    PloS one

    2014  Volume 9, Issue 1, Page(s) e86660

    Abstract: The origin of wound repair macrophages is incompletely defined and was examined here in sterile wounds using the subcutaneous polyvinyl alcohol sponge implantation model in mice. Phenotypic analysis identified F4/80(+)Ly6C(hi)CD64(+)MerTK(-) monocytes ... ...

    Abstract The origin of wound repair macrophages is incompletely defined and was examined here in sterile wounds using the subcutaneous polyvinyl alcohol sponge implantation model in mice. Phenotypic analysis identified F4/80(+)Ly6C(hi)CD64(+)MerTK(-) monocytes and F4/80(+)Ly6C(low)CD64(+)MerTK(+) macrophages in the wound. Circulating monocytes were the precursors of inflammatory Ly6C(hi) wound monocytes. Ly6C(low)MerTK(+) macrophages appeared later, expressed CD206, CD11c, and MHC class II, produced cytokines consistent with repair function, and lacked a gene expression profile compatible with mesenchymal transition or fibroblastic transdifferentiation. Data also demonstrated that Ly6C(hi) wound cells were precursors of Ly6C(low) macrophages, although monocytes did not undergo rapid maturation but rather persisted in the wound as Ly6C(hi)MerTK(-) cells. MerTK-deficient mice were examined to determine whether MerTK-dependent signals from apoptotic cells regulated the maturation of wound macrophages. MerTK-deficient mice had day 14 cell compositions that resembled more immature wounds, with a smaller proportion of F4/80(+) cells and higher frequencies of Ly6G(+) neutrophils and Ly6C(hi) monocytes. The cytokine profile and number of apoptotic cells in day 14 wounds of MerTK-deficient mice was unaffected despite the alterations in cell composition. Overall, these studies identified a differentiation pathway in response to sterile inflammation in which monocytes recruited from the circulation acquire proinflammatory function, persist in the wound, and mature into repair macrophages.
    MeSH term(s) Animals ; Antigens, Surface/metabolism ; Cell Differentiation ; Cytokines/biosynthesis ; Female ; Gene Expression Profiling ; Immunophenotyping ; Macrophages/cytology ; Macrophages/immunology ; Macrophages/metabolism ; Male ; Mice ; Monocytes/cytology ; Monocytes/immunology ; Monocytes/metabolism ; Phenotype ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Receptor Protein-Tyrosine Kinases/genetics ; Receptor Protein-Tyrosine Kinases/metabolism ; Time Factors ; Wounds and Injuries/genetics ; Wounds and Injuries/immunology ; Wounds and Injuries/metabolism ; c-Mer Tyrosine Kinase
    Chemical Substances Antigens, Surface ; Cytokines ; Proto-Oncogene Proteins ; Mertk protein, mouse (EC 2.7.10.1) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; c-Mer Tyrosine Kinase (EC 2.7.10.1)
    Language English
    Publishing date 2014-01-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0086660
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Toll-like receptor 4 signaling regulates the acute local inflammatory response to injury and the fibrosis/neovascularization of sterile wounds.

    Brancato, Samielle K / Thomay, Alan A / Daley, Jean M / Crane, Meredith J / Reichner, Jonathan S / Sabo, Edmond / Albina, Jorge E

    Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society

    2013  Volume 21, Issue 4, Page(s) 624–633

    Abstract: The role of Toll-like receptor 4 (TLR4) in the regulation of inflammation and fibrosis in sterile wounds was investigated in TLR4 signal-deficient (C3H/HeJ or TLR4(-/-) ) and control mice using the subcutaneously implanted polyvinyl alcohol sponge wound ... ...

    Abstract The role of Toll-like receptor 4 (TLR4) in the regulation of inflammation and fibrosis in sterile wounds was investigated in TLR4 signal-deficient (C3H/HeJ or TLR4(-/-) ) and control mice using the subcutaneously implanted polyvinyl alcohol sponge wound model. Total and differential wound cell counts 1, 3, and 7 days after injury did not differ between C3H/HeJ and C3H/HeOuJ animals. Blood monocytes from both strains expressed CCR2 equally. Day one wounds in C3H/HeJ mice contained fewer Gr-1(high) wound macrophages, CCL3, and CCL5, and more CCL17 than those in controls. The accumulation of CCL2, CX3CL1, tumor necrosis factor-α, interleukin (IL)-6, IL-10, IL-12, and interferon-γ in wound fluids was not TLR4 dependent. Wound macrophages from C3H/HeJ and C3H/HeOuJ mice expressed CCR4 and CCR5, but not CCR1 or CCR3. Wound macrophage recruitment was not altered in CCR5(-/-) mice or in C3H/HeOuJ animals injected with neutralizing anti-CCL3 and anti-CCL5 antibodies. Neutralization of the CCR4 ligand CCL17 in C3H/HeJ mice did not alter wound macrophage populations. There was a twofold increase in collagen content and number of neovessels in 21-day-old wounds in C3H/HeJ vs. C3H/HeOuJ mice. There were no differences between strains in the number of myofibroblasts in the wounds 7 or 21 days postwounding. The increased fibrosis and angiogenesis in wounds from /HeJ mice correlated with higher concentrations of transforming growth factor-β and fibroblast growth factor 2 in wound fluids from these animals. Wound fluids did not contain detectable lipopolysaccharide and did not induce IκBα degradation in J774.A1 macrophages. Results support a role for endogenous ligands of TLR4 in the regulation of inflammation and repair in sterile wounds.
    MeSH term(s) Animals ; Chemokine CCL2/immunology ; Chemokine CCL3/immunology ; Chemokine CCL5/immunology ; Chemokine CX3CL1/immunology ; Disease Progression ; Fibroblast Growth Factor 2/metabolism ; Fibrosis/immunology ; Interferon-gamma/immunology ; Interleukin-10/immunology ; Interleukin-12/immunology ; Interleukin-6/immunology ; Macrophages/immunology ; Mice ; Mice, Inbred C3H ; Mice, Transgenic ; Myofibroblasts/cytology ; Neovascularization, Physiologic/immunology ; Polyvinyl Alcohol ; Signal Transduction ; Toll-Like Receptor 4/immunology ; Transforming Growth Factor beta1/metabolism ; Tumor Necrosis Factor-alpha/immunology ; Wound Healing/immunology ; Wounds and Injuries/immunology
    Chemical Substances Ccl2 protein, mouse ; Ccl3 protein, mouse ; Ccl5 protein, mouse ; Chemokine CCL2 ; Chemokine CCL3 ; Chemokine CCL5 ; Chemokine CX3CL1 ; Cx3cl1 protein, mouse ; IL10 protein, mouse ; Interleukin-6 ; Tlr4 protein, mouse ; Toll-Like Receptor 4 ; Transforming Growth Factor beta1 ; Tumor Necrosis Factor-alpha ; interleukin-6, mouse ; Fibroblast Growth Factor 2 (103107-01-3) ; Interleukin-10 (130068-27-8) ; Interleukin-12 (187348-17-0) ; Interferon-gamma (82115-62-6) ; Polyvinyl Alcohol (9002-89-5)
    Language English
    Publishing date 2013-06-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1174873-4
    ISSN 1524-475X ; 1067-1927
    ISSN (online) 1524-475X
    ISSN 1067-1927
    DOI 10.1111/wrr.12061
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    Zs.A 3890: Show issues Location:
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  5. Article ; Online: The phenotype of murine wound macrophages.

    Daley, Jean M / Brancato, Samielle K / Thomay, Alan A / Reichner, Jonathan S / Albina, Jorge E

    Journal of leukocyte biology

    2010  Volume 87, Issue 1, Page(s) 59–67

    Abstract: The phenotype of wound macrophages has not been studied by direct examination of these cells, yet macrophages recruited to sites of injury are described as alternatively activated macrophages, requiring IL-4 or IL-13 for phenotypic expression. This study ...

    Abstract The phenotype of wound macrophages has not been studied by direct examination of these cells, yet macrophages recruited to sites of injury are described as alternatively activated macrophages, requiring IL-4 or IL-13 for phenotypic expression. This study characterized wound macrophage phenotype in the PVA sponge wound model in mice. Eighty-five percent of wound macrophages isolated 1 day after injury expressed Gr-1, but only 20% of those isolated at 7 days expressed this antigen. Macrophages from 1-, 3-, and 7-day wounds expressed markers of alternative activation,including mannose receptor, dectin-1, arginase 1,and Ym1, but did not contain iNOS. Day 1 wound macrophages produced more TNF-alpha, more IL-6, and less TGF-beta than Day 7 wound macrophages. Wound macrophages did not produce IL-10. The cytokines considered necessary for alternative activation of macrophages,IL-4 and IL-13, were not detected in the wound environment and were not produced by wound cells.Wound macrophages did not contain PStat6. Wound fluids inhibited IL-13-dependent phosphorylation of Stat6 and contained IL-13Ralpha2, a soluble decoy receptor for IL-13. The phenotype of wound macrophages was not altered in mice lacking IL-4Ralpha, which is required for Stat6-dependent signaling of IL-4 and IL-13.Wound macrophages exhibit a complex phenotype,which includes traits associated with alternative and classical activation and changes as the wound matures.The wound macrophage phenotype does not require IL-4 or IL-13.
    MeSH term(s) Animals ; Biomarkers ; Cytokines/analysis ; Exudates and Transudates/chemistry ; Foreign Bodies/pathology ; Gelatin Sponge, Absorbable ; Interleukin-13/physiology ; Interleukin-4/physiology ; Lectins, C-Type/analysis ; Macrophage Activation ; Macrophages/chemistry ; Macrophages/physiology ; Male ; Mannose-Binding Lectins/analysis ; Membrane Proteins/analysis ; Mice ; Mice, Knockout ; Nerve Tissue Proteins/analysis ; Phenotype ; Phosphorylation ; Protein Processing, Post-Translational ; Receptors, Cell Surface/analysis ; Receptors, Cell Surface/deficiency ; Receptors, Cell Surface/physiology ; Receptors, Chemokine/analysis ; STAT6 Transcription Factor/metabolism ; Skin/injuries ; Specific Pathogen-Free Organisms ; Wound Healing/physiology
    Chemical Substances Biomarkers ; Cytokines ; Gr-1 protein, mouse ; Il4ra protein, mouse ; Interleukin-13 ; Lectins, C-Type ; Mannose-Binding Lectins ; Membrane Proteins ; Nerve Tissue Proteins ; Receptors, Cell Surface ; Receptors, Chemokine ; STAT6 Transcription Factor ; Stat6 protein, mouse ; dectin 1 ; mannose receptor ; Interleukin-4 (207137-56-2)
    Language English
    Publishing date 2010-01-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 605722-6
    ISSN 1938-3673 ; 0741-5400
    ISSN (online) 1938-3673
    ISSN 0741-5400
    DOI 10.1189/jlb.0409236
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