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      Catecholamine stress alters neutrophil trafficking and impairs wound healing by β 2 adrenergic receptor mediated upregulation of IL-6

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          Abstract

          Stress-induced hormones can alter the inflammatory response to tissue injury, however, the precise mechanism by which epinephrine influences inflammatory response and wound healing is not well defined. Here we demonstrate that epinephrine alters the neutrophil (PMN)-dependent inflammatory response to a cutaneous wound. Using non-invasive real-time imaging of genetically-tagged PMNs in a murine skin wound, chronic, epinephrine-mediated stress was modeled by sustained delivery of epinephrine. Prolonged systemic exposure of epinephrine resulted in persistent PMN trafficking to the wound site via an IL-6 mediated mechanism, and this in turn impaired wound repair. Further, we demonstrate that β 2 adrenergic receptor-dependent activation of pro-inflammatory macrophages is critical for epinephrine-mediated IL-6 production. This study expands our current understanding of stress hormone-mediated impairment of wound healing and provides an important mechanistic link to explain how epinephrine stress exacerbates inflammation via increased number and lifetime of PMNs.

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          Wound healing: an overview of acute, fibrotic and delayed healing.

          Robert F. Diegelmann, Melissa Evans (2004)
          Acute wounds normally heal in a very orderly and efficient manner characterized by four distinct, but overlapping phases: hemostasis, inflammation, proliferation and remodeling. Specific biological markers characterize healing of acute wounds. Likewise, unique biologic markers also characterize pathologic responses resulting in fibrosis and chronic non-healing ulcers. This review describes the major biological processes associated with both normal and pathologic healing. The normal healing response begins the moment the tissue is injured. As the blood components spill into the site of injury, the platelets come into contact with exposed collagen and other elements of the extracellular matrix. This contact triggers the platelets to release clotting factors as well as essential growth factors and cytokines such as platelet-derived growth factor (PDGF) and transforming growth factor beta (TGF-beta). Following hemostasis, the neutrophils then enter the wound site and begin the critical task of phagocytosis to remove foreign materials, bacteria and damaged tissue. As part of this inflammatory phase, the macrophages appear and continue the process of phagocytosis as well as releasing more PDGF and TGF beta. Once the wound site is cleaned out, fibroblasts migrate in to begin the proliferative phase and deposit new extracellular matrix. The new collagen matrix then becomes cross-linked and organized during the final remodeling phase. In order for this efficient and highly controlled repair process to take place, there are numerous cell-signaling events that are required. In pathologic conditions such as non-healing pressure ulcers, this efficient and orderly process is lost and the ulcers are locked into a state of chronic inflammation characterized by abundant neutrophil infiltration with associated reactive oxygen species and destructive enzymes. Healing proceeds only after the inflammation is controlled. On the opposite end of the spectrum, fibrosis is characterized by excessive matrix deposition and reduced remodeling. Often fibrotic lesions are associated with increased densities of mast cells. By understanding the functional relationships of these biological processes of normal compared to abnormal wound healing, hopefully new strategies can be designed to treat the pathological conditions.
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            β-Adrenergic receptor antagonism prevents anxiety-like behavior and microglial reactivity induced by repeated social defeat.

            Eric Wohleb, Mark L. Hanke, Angela W Corona … (2011)
            Psychosocial stress is associated with altered immune function and development of psychological disorders including anxiety and depression. Here we show that repeated social defeat in mice increased c-Fos staining in brain regions associated with fear and threat appraisal and promoted anxiety-like behavior in a β-adrenergic receptor-dependent manner. Repeated social defeat also significantly increased the number of CD11b(+)/CD45(high)/Ly6C(high) macrophages that trafficked to the brain. In addition, several inflammatory markers were increased on the surface of microglia (CD14, CD86, and TLR4) and macrophages (CD14 and CD86) after social defeat. Repeated social defeat also increased the presence of deramified microglia in the medial amygdala, prefrontal cortex, and hippocampus. Moreover, mRNA analysis of microglia indicated that repeated social defeat increased levels of interleukin (IL)-1β and reduced levels of glucocorticoid responsive genes [glucocorticoid-induced leucine zipper (GILZ) and FK506 binding protein-51 (FKBP51)]. The stress-dependent changes in microglia and macrophages were prevented by propranolol, a β-adrenergic receptor antagonist. Microglia isolated from socially defeated mice and cultured ex vivo produced markedly higher levels of IL-6, tumor necrosis factor-α, and monocyte chemoattractant protein-1 after stimulation with lipopolysaccharide compared with microglia from control mice. Last, repeated social defeat increased c-Fos activation in IL-1 receptor type-1-deficient mice, but did not promote anxiety-like behavior or microglia activation in the absence of functional IL-1 receptor type-1. These findings indicate that repeated social defeat-induced anxiety-like behavior and enhanced reactivity of microglia was dependent on activation of β-adrenergic and IL-1 receptors.
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              Long-Term Persistance of the Pathophysiologic Response to Severe Burn Injury

              Marc Jeschke, Gerd Gauglitz, Gabriela Kulp … (2011)
              Background Main contributors to adverse outcomes in severely burned pediatric patients are profound and complex metabolic changes in response to the initial injury. It is currently unknown how long these conditions persist beyond the acute phase post-injury. The aim of the present study was to examine the persistence of abnormalities of various clinical parameters commonly utilized to assess the degree hypermetabolic and inflammatory alterations in severely burned children for up to three years post-burn to identify patient specific therapeutic needs and interventions. Methodology/Principal Findings Patients: Nine-hundred seventy-seven severely burned pediatric patients with burns over 30% of the total body surface admitted to our institution between 1998 and 2008 were enrolled in this study and compared to a cohort non-burned, non-injured children. Demographics and clinical outcomes, hypermetabolism, body composition, organ function, inflammatory and acute phase responses were determined at admission and subsequent regular intervals for up to 36 months post-burn. Statistical analysis was performed using One-way ANOVA, Student's t-test with Bonferroni correction where appropriate with significance accepted at p<0.05. Resting energy expenditure, body composition, metabolic markers, cardiac and organ function clearly demonstrated that burn caused profound alterations for up to three years post-burn demonstrating marked and prolonged hypermetabolism, p<0.05. Along with increased hypermetabolism, significant elevation of cortisol, catecholamines, cytokines, and acute phase proteins indicate that burn patients are in a hyperinflammatory state for up to three years post-burn p<0.05. Conclusions Severe burn injury leads to a much more profound and prolonged hypermetabolic and hyperinflammatory response than previously shown. Given the tremendous adverse events associated with the hypermetabolic and hyperinflamamtory responses, we now identified treatment needs for severely burned patients for a much more prolonged time.
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 0426720
                Journal ID (pubmed-jr-id): 4839
                Journal ID (nlm-ta): J Invest Dermatol
                Journal ID (iso-abbrev): J. Invest. Dermatol.
                Title: The Journal of investigative dermatology
                ISSN (Print): 0022-202X
                ISSN (Electronic): 1523-1747
                Publication date Nihms-submitted: 11 December 2013
                Publication date (Electronic): 11 October 2013
                Publication date (Print): March 2014
                Publication date PMC-release: 01 September 2014
                Volume: 134
                Issue: 3
                Pages: 809-817
                Affiliations
                [1 ]Department of Biomedical Engineering, University of California at Davis, Davis, CA 95616 USA
                [2 ]Department of Dermatology, University of California at Davis School of Medicine, Davis, CA 95616 USA
                [3 ]School of Veterinary Medicine: Pathology, Microbiology, Immunology, University of California at Davis School of Veterinary Medicine, Davis, CA 95616 US
                [4 ]Department of Biological Sciences, Kent State University, Kent, OH 44242 USA
                [5 ]Shriners Hospital of Northern California, Sacramento CA 95817 USA
                [6 ]Dermatology Section, Department of Veterans Affairs, Northern California Health Care System, Mather, CA 95655 USA
                Author notes
                Corresponding author: R. Rivkah Isseroff, Department of Dermatology, University of California at Davis, Davis, CA 95616, Phone: 530-752-9767, Fax: 530-752-9766, rrisseroff@ 123456ucdavis.edu
                Article
                Manuscript ID: NIHMS527667
                DOI: 10.1038/jid.2013.415
                PMC ID: 4013292
                PubMed ID: 24121404
                SO-VID: 64164f4e-1ece-4268-9eed-ab9be3b8f066
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                ScienceOpen disciplines: Dermatology
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                ScienceOpen disciplines: Dermatology

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