Psychoneuroimmunology: The interface between behavior, brain, and immunity.

Maier, Steven F.; Watkins, Linda R.; Fleshner, Monika

doi:10.1037/0003-066x.49.12.1004

Cited by 326 publications

(186 citation statements)

References 83 publications

(100 reference statements)

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“…The reference lists of 11 review articles on stress and the immune system (Benschop, Geenen, et al, 1998;Biondi, 2001;Cacioppo, 1994;S. Cohen & Herbert, 1996;Herbert & Cohen, 1993;Kiecolt-Glaser, Cacioppo, Malarkey, & Glaser, 1992;Kiecolt-Glaser, McGuire, Robles, & Glaser, 2002;Maier, Watkins, & Fleshner, 1994;O'Leary, 1990;Zorrilla et al, 2001) were then searched to identify additional articles.We selected only articles that met a number of inclusion criteria. The first criterion was that the work had to include a measure of stress.…”

mentioning

confidence: 99%

Psychological Stress and the Human Immune System: A Meta-Analytic Study of 30 Years of Inquiry.

Segerstrom

Miller

2004

Psychological Bulletin

2,647

1,845

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The present report meta-analyzes more than 300 empirical articles describing a relationship between psychological stress and parameters of the immune system in human participants. Acute stressors (lasting minutes) were associated with potentially adaptive upregulation of some parameters of natural immunity and downregulation of some functions of specific immunity. Brief naturalistic stressors (such as exams) tended to suppress cellular immunity while preserving humoral immunity. Chronic stressors were associated with suppression of both cellular and humoral measures. Effects of event sequences varied according to the kind of event (trauma vs. loss). Subjective reports of stress generally did not associate with immune change. In some cases, physical vulnerability as a function of age or disease also increased vulnerability to immune change during stressors.Since the dawn of time, organisms have been subject to evolutionary pressure from the environment. The ability to respond to environmental threats or stressors such as predation or natural disaster enhanced survival and therefore reproductive capacity, and physiological responses that supported such responses could be selected for. In mammals, these responses include changes that increase the delivery of oxygen and glucose to the heart and the large skeletal muscles. The result is physiological support for adaptive behaviors such as "fight or flight." Immune responses to stressful situations may be part of these adaptive responses because, in addition to the risk inherent in the situation (e.g., a predator), fighting and fleeing carries the risk of injury and subsequent entry of infectious agents into the bloodstream or skin. Any wound in the skin is likely to contain pathogens that could multiply and cause infection (Williams & Leaper, 1998). Stress-induced changes in the immune system that could accelerate wound repair and help prevent infections from taking hold would therefore be adaptive and selected along with other physiological changes that increased evolutionary fitness.Modern humans rarely encounter many of the stimuli that commonly evoked fight-or-flight responses for their ancestors, such as predation or inclement weather without protection. However, human physiological response continues to reflect the demands of earlier environments. Threats that do not require a physical response (e.g., academic exams) may therefore have physical consequences, including changes in the immune system. Indeed, over the past 30 years, more than 300 studies have been done on stress and immunity in humans, and together they have shown that psychological challenges are capable of modifying various features of the immune response. In this article we attempt to consolidate empirical knowledge about psychological stress and the human immune system through meta-analysis. Both the construct of stress and the human immune system are complex, and both could consume bookCorrespondence concerning this article should be addressed to Suzanne C. Segerstrom, Department of Ps...

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confidence: 99%

Psychological Stress and the Human Immune System: A Meta-Analytic Study of 30 Years of Inquiry.

Segerstrom

Miller

2004

Psychological Bulletin

2,647

1,845

View full text Add to dashboard Cite

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“…A lthough it has long been apparent that the immune system and the brain are closely connected, and rapid progress in our understanding of the molecules involved in regulating both immune and neural functions has been made, the extent and the exact mechanisms of this connection are still matters of considerable debate (1). One of the most likely mediators for communication between these two systems is the cytokine network because both neural and immune cells express cytokine receptors that regulate numerous aspects of cell function such as survival, differentiation, and motility.…”

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confidence: 99%

Cytokine signaling through the JAK/STAT pathway is required for long-term memory in Drosophila

Copf

Goguel²,

Lampin-Saint-Amaux³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Cytokine signaling through the JAK/STAT pathway regulates multiple cellular responses, including cell survival, differentiation, and motility. Although significant attention has been focused on the role of cytokines during inflammation and immunity, it has become clear that they are also implicated in normal brain function. However, because of the large number of different genes encoding cytokines and their receptors in mammals, the precise role of cytokines in brain physiology has been difficult to decipher. Here, we took advantage of Drosophila's being a genetically simpler model system to address the function of cytokines in memory formation. Expression analysis showed that the cytokine Upd is enriched in the Drosophila memory center, the mushroom bodies. Using tissue-and adult-specific expression of RNAi and dominantnegative proteins, we show that not only is Upd specifically required in the mushroom bodies for olfactory aversive long-term memory but the Upd receptor Dome, as well as the Drosophila JAK and STAT homologs Hop and Stat92E, are also required, while being dispensable for less stable memory forms.

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“…Stress is suspected to play a role in the etiology of many diseases, and numerous elegant studies have shown that stress can be immunosuppressive and, hence, may be detrimental to health (5)(6)(7)(8)(9)(10)(11)(12). However, we have suggested that, under certain conditions, a stress response may enhance immune function and prepare the immune system for challenges (e.g., wounding or infection) that may be imposed by a stressor, just as a stress response prepares the nervous, cardiovascular, musculoskeletal, and neuroendocrine systems for fight or flight (1,3,(13)(14)(15).…”

mentioning

confidence: 99%

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

Dhabhar

Satoskar

Bluethmann

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

144

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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.

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Psychoneuroimmunology: The interface between behavior, brain, and immunity.

Cited by 326 publications

References 83 publications

Psychological Stress and the Human Immune System: A Meta-Analytic Study of 30 Years of Inquiry.

Psychological Stress and the Human Immune System: A Meta-Analytic Study of 30 Years of Inquiry.

Cytokine signaling through the JAK/STAT pathway is required for long-term memory in Drosophila

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

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