Stress-induced enhancement of skin immune function: A role for γ interferon

Abstract

Contrary to the widespread belief that stress is necessarily immunosuppressive, recent studies have shown that, under certain conditions, stress can induce a significant enhancement of a skin cellmediated immune response [delayed-type hypersensitivity (DTH) or contact hypersensitivity]. Adrenal stress hormones and a stressinduced trafficking of leukocytes from the blood to the skin have been identified as systemic mediators of this immunoenhancement. Because ␥ interferon (IFN␥) is an important cytokine mediator of DTH, the studies described here were designed to examine its role as a local mediator of the stress-induced enhancement of skin DTH. The effect of acute stress on skin DTH was examined in wild-type and IFN␥ receptor-deficient (IFN␥R؊͞؊) mice that had previously been sensitized with 2,4-dinitro-1-fluorobenzene. Acutely stressed wild-type mice showed a significantly larger DTH response than nonstressed mice. In contrast, IFN␥R؊͞؊ mice failed to show a stress-induced enhancement of skin DTH. Immunoneutralization of IFN␥ in wild-type mice significantly reduced the stress-induced enhancement of skin DTH. In addition, an inflammatory response induced by direct IFN␥ administration to the skin was significantly enhanced by acute stress. Our results suggest that IFN␥ is an important local mediator of a stress-induced enhancement of skin DTH. These studies are clinically relevant because, depending on the nature of the antigen, DTH reactions mediate numerous protective (e.g., resistance to viral, bacterial, parasitic, and fungal infections) or pathological (e.g., autoimmune reactions and contact sensitivity reactions such as that to poison ivy) immune responses.

Osteopontin: Role in immune regulation and stress responses

“…Both HU and CRS are physical stress models containing a significant psychological component that activates neural transmitters and stress hormones (Aviles et al, 2005;Dhabhar et al, 2000). Until now, the role of OPN in the stress response of immune organs has not been examined.…”

“…Stress hormones such as cortisol play a pivotal role in modulating pro/anti-inflammatory responses and the TH1/Th2 cytokine balance, thereby influencing the susceptibility to and outcome of various immune-related diseases (Calcagni and Elenkov, 2006). While chronic stress is immunosuppressive and leads to increased vulnerability to infections and cancer, acute stress promotes immunoprotection through cell-mediated immunity (Dhabhar et al, 2000, Viswanathan et al, 2005.…”

Pineal-dependent and -independent effects of photoperiod on immune function in Siberian hamsters (Phodopus sungorus)

“…Circulating lymphocyte concentrations (e.g., T cells, B cells) are greater in short days relative to long days (Bilbo et al, 2002a;Prendergast et al, 2004a;Yellon et al, 2005). In addition, more integrative measures of immune function such as T-cell-dependent skin inflammatory responses, which depend in part on specific leukocyte subtypes (i.e., CD44+ and CD62+ leukocytes), are greater in short days relative to long days (Dhabhar et al, 2000;Bilbo et al, 2002a;Prendergast et al, 2004a). Short days also ameliorate the acute-phase symptoms of bacterial infection in Siberian hamsters: LPS-induced IL-1β, IL-6, and TNF-α production are lower (Bilbo et al, 2002b;Prendergast et al, 2003a), and the magnitude and/or persistence of thermoregulatory (fever), behavioral (anorexia), emotional (anhedonia), and ponderal (cachexia) responses to simulated infection are attenuated (Bilbo et al, 2002b).…”

The neurobiology of stress: from serendipity to clinical relevance11Published on the World Wide Web on 22 November 2000.

“…2). Dexamethasone, [30]. Furthermore, immunoneutralization of IFN gamma in which does not bind to serum corticosteroid binding normal mice also blocks the stress effect.…”