Restraint stress alters neutrophil and macrophage phenotypes during wound healing

[1]  K. Leung,et al.  Synthetic decapeptide reduces bacterial load and accelerates healing in the wounds of restraint-stressed mice , 2012, Brain, Behavior, and Immunity.

[2]  Su-Ji Min,et al.  Major stress hormones suppress the response of macrophages through down-regulation of TLR2 and TLR4. , 2012, The Journal of surgical research.

[3]  R. Sesti-Costa,et al.  Chronic cold stress in mice induces a regulatory phenotype in macrophages: Correlation with increased 11β-hydroxysteroid dehydrogenase expression , 2012, Brain, Behavior, and Immunity.

[4]  T. Koh,et al.  Dysregulation of monocyte/macrophage phenotype in wounds of diabetic mice. , 2011, Cytokine.

[5]  D. Carroll,et al.  Altered Human Neutrophil Function in Response to Acute Psychological Stress , 2010, Psychosomatic medicine.

[6]  K. Khosrotehrani,et al.  Skin wound healing modulation by macrophages. , 2010, International journal of clinical and experimental pathology.

[7]  J. Sheridan,et al.  Social disruption induces lung inflammation , 2010, Brain, Behavior, and Immunity.

[8]  J. Albina,et al.  The phenotype of murine wound macrophages , 2010, Journal of leukocyte biology.

[9]  T. Connor,et al.  Psychological stress increases expression of IL-10 and its homolog IL-19 via β-adrenoceptor activation: Reversal by the anxiolytic chlordiazepoxide , 2009, Brain, Behavior, and Immunity.

[10]  J. Edwards,et al.  Exploring the full spectrum of macrophage activation , 2008, Nature Reviews Immunology.

[11]  N. Rosenthal,et al.  Overexpression of mIGF-1 in keratinocytes improves wound healing and accelerates hair follicle formation and cycling in mice. , 2008, The American journal of pathology.

[12]  N. Eijkelkamp,et al.  Restraint stress impairs early wound healing in mice via α-adrenergic but not β-adrenergic receptors , 2007, Brain, Behavior, and Immunity.

[13]  W. Nacken,et al.  Glucocorticoids induce differentiation of a specifically activated, anti-inflammatory subtype of human monocytes. , 2007, Blood.

[14]  Xia Zhang,et al.  Biochemical and functional characterization of three activated macrophage populations , 2006, Journal of leukocyte biology.

[15]  A. Mantovani,et al.  Differential regulation of chemokine production by Fcγ receptor engagement in human monocytes: association of CCL1 with a distinct form of M2 monocyte activation (M2b, Type 2) , 2006, Journal of leukocyte biology.

[16]  M. Ferguson,et al.  Cytokine gene expression in a murine wound healing model. , 2005, Cytokine.

[17]  N. Quan,et al.  Impaired wound contraction and delayed myofibroblast differentiation in restraint-stressed mice , 2005, Brain, Behavior, and Immunity.

[18]  Chandan K. Sen,et al.  Hyperbaric oxygen therapy ameliorates stress-impaired dermal wound healing , 2005, Brain, Behavior, and Immunity.

[19]  F. Dhabhar,et al.  Stress-induced enhancement of leukocyte trafficking into sites of surgery or immune activation. , 2005 .

[20]  Limin Zheng,et al.  Pathogen-Induced Apoptotic Neutrophils Express Heat Shock Proteins and Elicit Activation of Human Macrophages1 , 2004, The Journal of Immunology.

[21]  J. Palermo-neto,et al.  Effects of physical and psychological stressors on behavior, macrophage activity, and Ehrlich tumor growth , 2003, Brain, Behavior, and Immunity.

[22]  J. Sheridan,et al.  Restraint stress alters the expression of interleukin-1 and keratinocyte growth factor at the wound site: an in situ hybridization study , 2002, Journal of Neuroimmunology.

[23]  F. Dhabhar,et al.  Short day lengths augment stress-induced leukocyte trafficking and stress-induced enhancement of skin immune function , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[24]  E. Fisher,et al.  Laser capture microdissection analysis of gene expression in macrophages from atherosclerotic lesions of apolipoprotein E-deficient mice , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[25]  David A. Padgett,et al.  Stress-Induced Susceptibility to Bacterial Infection During Cutaneous Wound Healing , 2002, Brain, Behavior, and Immunity.

[26]  J. Pfeilschifter,et al.  Large and sustained induction of chemokines during impaired wound healing in the genetically diabetic mouse: prolonged persistence of neutrophils and macrophages during the late phase of repair. , 2000, The Journal of investigative dermatology.

[27]  J. A. Hobden,et al.  Macrophage Inflammatory Protein-2 Is a Mediator of Polymorphonuclear Neutrophil Influx in Ocular Bacterial Infection1 , 2000, The Journal of Immunology.

[28]  J. M. Cousin,et al.  Glucocorticoids promote nonphlogistic phagocytosis of apoptotic leukocytes. , 1999, Journal of immunology.

[29]  E. Bröcker,et al.  Chemokines IL-8, GROalpha, MCP-1, IP-10, and Mig are sequentially and differentially expressed during phase-specific infiltration of leukocyte subsets in human wound healing. , 1998, The American journal of pathology.

[30]  B. Wang,et al.  Restraint stress-induced immunosuppression by inhibiting leukocyte migration and Th1 cytokine expression during the intraperitoneal infection of Listeria monocytogenes , 1998, Journal of Neuroimmunology.

[31]  H. Herschman,et al.  The murine neutrophil‐chemoattractant chemokines LIX, KC, and MIP‐2 have distinct induction kinetics, tissue distributions, and tissue‐specific sensitivities to glucocorticoid regulation in endotoxemia , 1998, Journal of leukocyte biology.

[32]  M. Burdick,et al.  MIP-1alpha as a critical macrophage chemoattractant in murine wound repair. , 1998, The Journal of clinical investigation.

[33]  J. Sheridan,et al.  Restraint Stress Slows Cutaneous Wound Healing in Mice , 1998, Brain, Behavior, and Immunity.

[34]  W. Busse,et al.  Cytokine profiles of stimulated blood lymphocytes in asthmatic and healthy adolescents across the school year. , 1997, Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research.

[35]  Y. Payette,et al.  Glucocorticoid receptor regulates expression of L-selectin and CD11/CD18 on human neutrophils. , 1997, Circulation.

[36]  J. Savill.  Apoptosis in resolution of inflammation , 1997, Journal of leukocyte biology.

[37]  K. Kishihara,et al.  Restraint stress-induced elevation of endogenous glucocorticoid suppresses migration of granulocytes and macrophages to an inflammatory locus , 1997, Journal of Neuroimmunology.

[38]  K. Watanabe,et al.  A stress-sensitive chemokinergic neuronal pathway in the hypothalamo-pituitary system , 1996, Neuroscience.

[39]  A. Beaudet,et al.  Infectious susceptibility and severe deficiency of leukocyte rolling and recruitment in E-selectin and P-selectin double mutant mice , 1996, The Journal of experimental medicine.

[40]  W. Fung-Leung,et al.  Tepoxalin blocks neutrophil migration into cutaneous inflammatory sites by inhibiting Mac‐1 and E‐selectin expression , 1996, European journal of immunology.

[41]  A. Bylund-Fellenius,et al.  Improved method for quantification of tissue PMN accumulation measured by myeloperoxidase activity. , 1990, Journal of pharmacological methods.

[42]  T. Springer,et al.  Tissue distribution, structural characterization, and biosynthesis of Mac-3, a macrophage surface glycoprotein exhibiting molecular weight heterogeneity. , 1983, The Journal of biological chemistry.

[43]  Alberto Mantovani,et al.  Macrophage activation and polarization. , 2008, Frontiers in bioscience : a journal and virtual library.

[44]  C. Haslett,et al.  MECHANISMS OF STEROID ACTION AND RESISTANCE IN INFLAMMATION Glucocorticoid-mediated regulation of granulocyte apoptosis and macrophage phagocytosis of apoptotic cells: implications for the resolution of inflammation , 2003 .

[45]  W. Seeger,et al.  Monocytes recruited into the alveolar air space of mice show a monocytic phenotype but upregulate CD14. , 2001, American journal of physiology. Lung cellular and molecular physiology.