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  1. AU="Henry, William L"
  2. AU="Lawless, Aleigha R"
  3. AU="Mora-Ríos, Félix Gustavo"

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  1. Article ; Online: Assessment of Acute Wound Healing using the Dorsal Subcutaneous Polyvinyl Alcohol Sponge Implantation and Excisional Tail Skin Wound Models.

    Crane, Meredith J / Henry, William L / Tran, Holly L / Albina, Jorge E / Jamieson, Amanda M

    Journal of visualized experiments : JoVE

    2020  , Issue 157

    Abstract: Wound healing is a complex process that requires the orderly progression of inflammation, granulation tissue formation, fibrosis, and resolution. Murine models provide valuable mechanistic insight into these processes; however, no single model fully ... ...

    Abstract Wound healing is a complex process that requires the orderly progression of inflammation, granulation tissue formation, fibrosis, and resolution. Murine models provide valuable mechanistic insight into these processes; however, no single model fully addresses all aspects of the wound healing response. Instead, it is ideal to use multiple models to address the different aspects of wound healing. Here, two different methods that address diverse aspects of the wound healing response are described. In the first model, polyvinyl alcohol sponges are subcutaneously implanted along the mouse dorsum. Following sponge retrieval, cells can be isolated by mechanical disruption, and fluids can be extracted by centrifugation, thus allowing for a detailed characterization of cellular and cytokine responses in the acute wound environment. A limitation of this model is the inability to assess the rate of wound closure. For this, a tail skin excision model is utilized. In this model, a 10 mm x 3 mm rectangular piece of tail skin is excised along the dorsal surface, near the base of the tail. This model can be easily photographed for planimetric analysis to determine healing rates and can be excised for histological analysis. Both described methods can be utilized in genetically altered mouse strains, or in conjunction with models of comorbid conditions, such as diabetes, aging, or secondary infection, in order to elucidate wound healing mechanisms.
    MeSH term(s) Acute Disease ; Animals ; Bandages ; Cell Separation ; Disease Models, Animal ; Inflammation/pathology ; Male ; Mice, Inbred C57BL ; Polyvinyl Alcohol/pharmacology ; Prostheses and Implants ; Skin/pathology ; Subcutaneous Tissue/drug effects ; Subcutaneous Tissue/pathology ; Tail/pathology ; Wound Healing/drug effects
    Chemical Substances Polyvinyl Alcohol (9002-89-5)
    Language English
    Publishing date 2020-03-25
    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. ; Video-Audio Media
    ZDB-ID 2259946-0
    ISSN 1940-087X ; 1940-087X
    ISSN (online) 1940-087X
    ISSN 1940-087X
    DOI 10.3791/60653
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Pulmonary influenza A virus infection leads to suppression of the innate immune response to dermal injury.

    Crane, Meredith J / Xu, Yun / Henry, William L / Gillis, Sean P / Albina, Jorge E / Jamieson, Amanda M

    PLoS pathogens

    2018  Volume 14, Issue 8, Page(s) e1007212

    Abstract: The innate immune system is responsible for many important functions in the body including responding to infection, clearing cancerous cells, healing wounds, and removing foreign substances. Although many of these functions happen simultaneously in life, ...

    Abstract The innate immune system is responsible for many important functions in the body including responding to infection, clearing cancerous cells, healing wounds, and removing foreign substances. Although many of these functions happen simultaneously in life, most laboratory studies of the innate immune response focus on one activity. How the innate immune system responds to concurrent insults in different parts of the body is not well understood. This study explores the impact of a lung infection on the cutaneous wound healing process. We used two complimentary models of injury: the excisional tail wound and subcutaneous implantation of polyvinyl alcohol (PVA) sponges. These models allow for assessment of the rate of closure and measurement of cellular and cytokine responses during acute wound healing, respectively. When mice with these healing wounds were infected with influenza A virus (IAV) in the lung there was a delay in wound healing. The viral lung infection suppressed the innate immune response in a healing wound, including cellular infiltrate, chemokines, growth factors, and cytokines. However, there was not a global immune suppression as there was an increase in inflammation systemically in mice with both infection and healing wounds compared to mice with only wounds or IAV infection. In addition, the lung immune response was largely unaffected indicating that responding to a lung infection is prioritized over a healing wound. This study introduces the concept of immune triage, in that when faced with multiple insults the immune system prioritizes responses. This paradigm likely applies to many situations that involve the innate immune system, and understanding how the innate immune system handles multiple insults is essential to understanding how it can efficiently clear pathogens while responding to other inflammatory events.
    MeSH term(s) Animals ; Immune Tolerance ; Immunity, Innate/physiology ; Influenza A virus/immunology ; Influenza A virus/pathogenicity ; Lung/virology ; Male ; Mice ; Mice, Inbred C57BL ; Orthomyxoviridae Infections/immunology ; Orthomyxoviridae Infections/virology ; Respiratory Tract Infections/immunology ; Respiratory Tract Infections/pathology ; Respiratory Tract Infections/virology ; Skin/immunology ; Skin/injuries ; Skin/virology ; Wound Healing/physiology
    Language English
    Publishing date 2018-08-23
    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.
    ZDB-ID 2205412-1
    ISSN 1553-7374 ; 1553-7366
    ISSN (online) 1553-7374
    ISSN 1553-7366
    DOI 10.1371/journal.ppat.1007212
    Database MEDical Literature Analysis and Retrieval System OnLINE

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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: Prostaglandin E2 suppresses lipopolysaccharide-stimulated IFN-beta production.

    Xu, X Julia / Reichner, Jonathan S / Mastrofrancesco, Balduino / Henry, William L / Albina, Jorge E

    Journal of immunology (Baltimore, Md. : 1950)

    2008  Volume 180, Issue 4, Page(s) 2125–2131

    Abstract: Macrophages activate the production of cytokines and chemokines in response to LPS through signaling cascades downstream from TLR4. Lipid mediators such as PGE(2), which are produced during inflammatory responses, have been shown to suppress MyD88- ... ...

    Abstract Macrophages activate the production of cytokines and chemokines in response to LPS through signaling cascades downstream from TLR4. Lipid mediators such as PGE(2), which are produced during inflammatory responses, have been shown to suppress MyD88-dependent gene expression upon TLR4 activation in macrophages. The study reported here investigated the effect of PGE(2) on TLR3- and TLR4-dependent, MyD88-independent gene expression in murine J774A.1 macrophages, as well as the molecular mechanism underlying such an effect. We demonstrate that PGE(2) strongly suppresses LPS-induced IFN-beta production at the mRNA and protein levels. Poly (I:C)-induced IFN-beta and LPS-induced CCL5 production were also suppressed by PGE(2). The inhibitory effect of PGE(2) on LPS-induced IFN-beta expression is mediated through PGE(2) receptor subtypes EP(2) and EP(4), and mimicked by the cAMP analog 8-Br-cAMP as well as by the adenylyl cyclase activator forskolin. The downstream effector molecule responsible for the cAMP-induced suppressive effect is exchange protein directly activated by cAMP (Epac) but not protein kinase A. Moreover, data demonstrate that Epac-mediated signaling proceeds through PI3K, Akt, and GSK3beta. In contrast, PGE(2) inhibits LPS-induced TNF-alpha production in these cells through a distinct pathway requiring protein kinase A activity and independent of Epac/PI3K/Akt. In vivo, administration of a cyclooxygenase inhibitor before LPS injection resulted in enhanced serum IFN-beta concentration in mice. Collectively, data demonstrate that PGE(2) is a negative regulator for IFN-beta production in activated macrophages and during endotoxemia.
    MeSH term(s) Animals ; Cell Line ; Dinoprostone/physiology ; Dose-Response Relationship, Immunologic ; Endotoxemia/immunology ; Endotoxemia/metabolism ; Gene Expression Regulation/immunology ; Interferon-beta/antagonists & inhibitors ; Interferon-beta/biosynthesis ; Interferon-beta/genetics ; Lipopolysaccharides/antagonists & inhibitors ; Lipopolysaccharides/pharmacology ; Macrophage Activation/immunology ; Macrophages/immunology ; Macrophages/metabolism ; Male ; Mice ; Myeloid Differentiation Factor 88/physiology ; RNA, Messenger/antagonists & inhibitors ; RNA, Messenger/biosynthesis ; Signal Transduction/immunology
    Chemical Substances Lipopolysaccharides ; Myd88 protein, mouse ; Myeloid Differentiation Factor 88 ; RNA, Messenger ; Interferon-beta (77238-31-4) ; Dinoprostone (K7Q1JQR04M)
    Language English
    Publishing date 2008-02-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.180.4.2125
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Modulation of macrophage phenotype by soluble product(s) released from neutrophils.

    Daley, Jean M / Reichner, Jonathan S / Mahoney, Eric J / Manfield, Laura / Henry, William L / Mastrofrancesco, Balduino / Albina, Jorge E

    Journal of immunology (Baltimore, Md. : 1950)

    2005  Volume 174, Issue 4, Page(s) 2265–2272

    Abstract: The regulation of macrophage phenotype by neutrophils was studied in the s.c. polyvinyl alcohol sponge wound model in mice made neutropenic by anti-Gr-1 Ab, as well as in cell culture. Wounds in neutropenic mice contained 100-fold fewer neutrophils than ... ...

    Abstract The regulation of macrophage phenotype by neutrophils was studied in the s.c. polyvinyl alcohol sponge wound model in mice made neutropenic by anti-Gr-1 Ab, as well as in cell culture. Wounds in neutropenic mice contained 100-fold fewer neutrophils than those in nonneutropenic controls 1 day after sponge implantation. Wound fluids from neutropenic mice contained 68% more TNF-alpha, 168% more IL-6, and 61% less TGF-beta1 than those from controls. Wound fluid IL-10 was not different between the two groups, and IL-4 was not detected. Intracellular TNF-alpha staining was greater in cells isolated from neutropenic wounds than in those from control wounds. The hypothesis that wound neutrophil products modulate macrophage phenotype was tested in Transwell cocultures of LPS-stimulated J774A.1 macrophages and day 1 wound cells (84% neutrophils/15% macrophages). Overnight cocultures accumulated 60% less TNF-alpha and IL-6 than cultures of J774A.1 alone. The suppression of cytokine release was mediated by a soluble factor(s), because culture supernatants from wound cells inhibited TNF-alpha and IL-6 release from LPS-stimulated J774A.1 cells. Culture supernatants from purified wound neutrophils equally suppressed TNF-alpha release from LPS-stimulated J774A.1 cells. Wound cell supernatants also suppressed TNF-alpha and superoxide release from murine peritoneal macrophages. The TNF-alpha inhibitory factor has a molecular mass <3000 Da and is neither PGE2 nor adenosine. The present findings confirm a role for neutrophils in the regulation of innate immune responses through modulation of macrophage phenotype.
    MeSH term(s) Animals ; Antibodies, Monoclonal/administration & dosage ; Antigens, Differentiation/immunology ; Biological Dressings ; Cell Line ; Cell Movement/immunology ; Cell-Free System/immunology ; Coculture Techniques ; Culture Media, Conditioned/metabolism ; Cytokines/antagonists & inhibitors ; Cytokines/biosynthesis ; Immunophenotyping ; Inflammation Mediators/metabolism ; Interleukin-6/antagonists & inhibitors ; Interleukin-6/metabolism ; Lipopolysaccharides/pharmacology ; Macrophages, Peritoneal/immunology ; Macrophages, Peritoneal/metabolism ; Macrophages, Peritoneal/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Neutropenia/immunology ; Neutrophils/immunology ; Neutrophils/metabolism ; Neutrophils/pathology ; Polyvinyl Alcohol ; Solubility ; Superoxides/metabolism ; Tumor Necrosis Factor-alpha/antagonists & inhibitors ; Tumor Necrosis Factor-alpha/biosynthesis ; Tumor Necrosis Factor-alpha/metabolism ; Wound Healing/immunology ; Wounds, Nonpenetrating/immunology ; Wounds, Nonpenetrating/pathology
    Chemical Substances Antibodies, Monoclonal ; Antigens, Differentiation ; Culture Media, Conditioned ; Cytokines ; Inflammation Mediators ; Interleukin-6 ; Lipopolysaccharides ; Tumor Necrosis Factor-alpha ; neutrophil differentiation antigens ; Superoxides (11062-77-4) ; Polyvinyl Alcohol (9002-89-5)
    Language English
    Publishing date 2005-02-08
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.174.4.2265
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Energy cost to the user

    Henry, William L

    Energy and public policy--1972 : a conference report from the Conference Board , p. 182-185

    1972  , Page(s) 182–185

    Author's details William L. Henry
    Publisher Conference Board]
    Publishing place [New York
    Document type Article
    Database ECONomics Information System

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