John F. Sheridan, PhD
Professor College of Dentistry
Phone number: (614) 688-4629
Efficient cutaneous wound healing quickly restores the protective barrier to injured tissue and reduces the risk of infection. Psychological stress is known to modulate inflammatory responses (Avitsur et al, 2007) and slow the healing of experimental cutaneous and mucosal wounds in humans (Kiecolt-Glaser, et al. 1998, Marucha et al., 1998). It has been shown that slowed healing is associated with activation of hypothalamic-pituitary-adrenal axis (HPA) and sympathetic nervous system (Padgett et al., 1998), which in turn is associated with diminished mononuclear cell trafficking (Padgett et al., 1998) and reduced expression of cytokine, chemokine and growth factor genes in wound tissue (Mercado et al., 2002). In addition, stress reduces oxygen content in wound tissue (Gajendrareddy et al, 2005) and increases the susceptibility to opportunistic bacterial infections (Rojas et al., 2003). Additional data generated thus far, have shown that stress alters inflammatory gene expression, fibroblast proliferation, angiogenesis, wound contraction and re-epithelialization. Thus, significant components of wound healing are negatively affected by stress-induced activation of neuroendocrine pathways and altered wound oxygen content. The goal of this project is to determine the mechanism by which psychological stress has a significant effect on chemokine, pro-inflammatory cytokine and growth factor gene expression during wound healing.
Nicole Powell, PhD, Research Scientist
LaTonia Stiner, PhD, Research Assistant Professor
Andrew Tarr, PhD, Postdoctoral Fellow
Brenda Reader, Predoctoral Fellow, IBGP
Eric Wohleb, Predoctoral Fellow, NSGP
Amanda Roloson, Predoctoral Fellow, IBGP
Neuroendocrine regulation of inflammation
Host repair of tissue damage
Immunity to viral and bacterial challenges
Padgett, D.A., Marucha, P.T., and Sheridan, J.F. Restraint stress slows cutaneous wound healing in mice. Brain, Behavior and Immunity 1998;12:64-73.
Padgett, D.A., Sheridan, J.F., Dorne, J., Bernston, G.G., Candelora, J., and Glaser, R. Social stress and the reactivation of latent herpes simplex virus-type 1. Proceedings of the National Academy of Science USA. 1998; 95:7231-7235.
Rojas, I.G., Padgett, D.A., Sheridan, J.F., and Marucha, P.M. Stress-induced susceptibility to bacterial infection during cutaneous wound healing. Brain, Behavior and Immunity 2002;16:74-84.
Avitsur, R., Stark, J.L., and Sheridan, J.F. Social stress induces glucocorticoid resistance in subordinate animals. Hormones and Behavior 2001;39:247-257.
Mercado, A.M., Padgett, D.A., Sheridan, J.F., and Marucha, P.T. Altered kinetics of IL-1α, IL-1β, and KGF-1 mRNA expression in early wounds of restrained mice. Brain, Behavior and Immunity 2002;16:150-162.
Sheridan, J.F., Padgett, D.A., Avitsur, R.A., and Marucha, P.T. Experimental models of stress and wound healing. J. World Surgery 2004;28:327-330.
Powell, N.D., Bailey, M.T., Mays, J.W., Stiner-Jones, L.M., Hanke, M.L., Padgett, D.A., and Sheridan, J.F. Repeated social defeat activates dendritic cells and enhances Toll-like receptor dependent cytokine secretion. Brain, Behavior and Immunity, 2008;23 (2):225-231.
Khoury, S.B., Thomas, L., Walters, J.D., Sheridan, J.F., and Leblebicioglu, B. Early wound healing following one-stage dental implant placement with and without antibiotic prophylaxis: A pilot study. J. Periodontology 2008; 79:1904-1912.
Cole, S.W., Arevalo, J.M., Takahasji, R., Sloan, E.K., Lutgendorf, S.K., Sood, A.K., Sheridan, J.F., and Seeman, T.E. Computational identification of gene-social environment interaction at the human IL6 locus. Proceedings of the National Academy of Science 2010;107(12): 5681-5686.
Wohleb, E., Hanke, M., Powell, N.D., Bailey, M.T., Nelson, R., Stiner, L.M., Corona, A., Godbout, J., & Sheridan, J.F. β2-Adrenergic receptor antagonism ameliorates anxiety-like behavior and microglial reactivity induced by repeated social defeat. Journal of Neuroscience 2011; 31:6277-6288.