Enhancement of Antigen-Specific Humoral and Cell-Mediated Immunity by Electric Footshock Stress in Rats

Wood, Paul G.; Karol, Meryl H.; Kusnecov, Alexander W.; Rabin, Bruce S.

doi:10.1006/brbi.1993.1014

Cited by 82 publications

(37 citation statements)

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“…Our data are consistent with those of other studies showing bidirectional effects of corticosterone on T cell proliferation (47) and stress-induced enhancements in in vitro parameters such as lymphocyte proliferation (48)(49)(50)(51), macrophage phagocytosis (52), natural killer cell activity (53,54), and cytokine production (55,56). Acute stress has also been shown to enhance skin DTH (57), accelerate antigen removal (58), and increase antigen-specific antibody titers in vivo (59)(60)(61)(62).…”

Section: Discussionsupporting

confidence: 91%

Enhancing versus suppressive effects of stress hormones on skin immune function

Dhabhar

McEwen

1999

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

571

414

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Delayed-type hypersensitivity (DTH) reactions are antigen-specific cell-mediated immune responses that, depending on the antigen, mediate beneficial (e.g., resistance to viruses, bacteria, and fungi) or harmful (e.g., allergic dermatitis and autoimmunity) aspects of immune function. Contrary to the idea that stress suppresses immunity, we have reported that short-duration stressors significantly enhance skin DTH and that a stress-induced trafficking of leukocytes to the skin may mediate this immunoenhancement. Here, we identify the hormonal mediators of a stressinduced enhancement of skin immunity. Adrenalectomy, which eliminates the glucocorticoid and epinephrine stress response, eliminated the stress-induced enhancement of skin DTH. Low-dose corticosterone or epinephrine administration significantly enhanced skin DTH and produced a significant increase in the number of T cells in lymph nodes draining the site of the DTH reaction. In contrast, high-dose corticosterone, chronic corticosterone, or low-dose dexamethasone administration significantly suppressed skin DTH. These results suggest a role for adrenal stress hormones as endogenous immunoenhancing agents. These results also show that hormones released during an acute stress response may help prepare the immune system for potential challenges (e.g., wounding or infection) for which stress perception by the brain may serve as an early warning signal.

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Section: Discussionsupporting

confidence: 91%

Enhancing versus suppressive effects of stress hormones on skin immune function

Dhabhar

McEwen

1999

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

571

414

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“…These studies also suggested that the effects of acute stress in this case were mediated primarily by norepinephrine [54] . Other investigators have similarly reported stress-induced enhancement of type-1 cytokine-driven CMI [55][56][57] and type-2 cytokine-driven humoral immunity [57,58] .…”

Section: Acute Stress-induced Enhancement Of Innate/ Primary Immune Rmentioning

confidence: 79%

Enhancing versus Suppressive Effects of Stress on Immune Function: Implications for Immunoprotection and Immunopathology

Dhabhar¹

2009

Neuroimmunomodulation

688

577

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Stress is known to suppress immune function and increase susceptibility to infections and cancer. Paradoxically, stress is also known to exacerbate asthma, and allergic, autoimmune and inflammatory diseases, although such diseases should be ameliorated by immunosuppression. Moreover, the short-term fight-or-flight stress response is one of nature’s fundamental defense mechanisms that enables the cardiovascular and musculoskeletal systems to promote survival, and it is unlikely that this response would suppress immune function at a time when it is most required for survival (e.g. in response to wounding and infection by a predator or aggressor). These observations suggest that stress may suppress immune function under some conditions while enhancing it under others. The effects of stress are likely to be beneficial or harmful depending on the type (immunoprotective, immunoregulatory/inhibitory, or immunopathological) of immune response that is affected. Studies have shown that several critical factors influence the direction (enhancing vs. suppressive) of the effects of stress or stress hormones on immune function: (1) Duration (acute vs. chronic) of stress: Acute or short-term stress experienced at the time of immune activation can enhance innate and adaptive immune responses. Chronic or long-term stress can suppress immunity by decreasing immune cell numbers and function and/or increasing active immunosuppressive mechanisms (e.g. regulatory T cells). Chronic stress can also dysregulate immune function by promoting proinflammatory and type-2 cytokine-driven responses. (2) Effects of stress on leukocyte distribution: Compartments that are enriched with immune cells during acute stress show immunoenhancement, while those that are depleted of leukocytes, show immunosuppression. (3) The differential effects of physiologic versus pharmacologic concentrations of glucocorticoids, and the differential effects of endogenous versus synthetic glucocorticoids: Endogenous hormones in physiological concentrations can have immunoenhancing effects. Endogenous hormones at pharmacologic concentrations, and synthetic hormones, are immunosuppressive. (4) The timing of stressor or stress hormone exposure relative to the time of activation and time course of the immune response: Immunoenhancement is observed when acute stress is experienced at early stages of immune activation, while immunosuppression may be observed at late stages of the immune response. We propose that it is important to study and, if possible, to clinically harness the immunoenhancing effects of the acute stress response, that evolution has finely sculpted as a survival mechanism, just as we study its maladaptive ramifications (chronic stress) that evolution has yet to resolve. In view of the ubiquitous nature of stress and its significant effects on immunoprotection as well as immunopathology, it is important to further elucidate the mechanisms mediating stress-immune interactions and to meaningfully translate findings from bench to bedside.

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“…However, a previous study had demonstrated that rats submitted immediately, and 24 hours after, immunization to a session of electrical foot-shocks (16 shocks, with 1.6 mA, 5s long, and 4 min interval), presented an increase in the humoral immune response (Wood et al, 1993). It must be pointed out that, in the present study, the stress session consisted of 5 shocks in the paws, with 1.6 mA, 2 s long, and 4 min interval.…”

Section: Discussionmentioning

confidence: 94%

The expression of an intraspecific aggressive reaction in the face of a stressor agent alters the immune response in rats

et al. 2005

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The repercussion on the immune response of the expression of intraspecific aggressiveness in the face of a stressor agent was investigated in rats. Ninety-day-old animals were divided into three groups: the control group (only immunological measurements were performed), the foot-shock (FS) (animals individually receiving FS), and the intraspecific aggressive response (IAR) group (animals receiving FS and presenting IAR). For immunological measurements, blood samples were collected promptly at 7 and 15 days after FS or IAR. The FS reduced the total leukocyte amount presented. However, aggressiveness triggered not only reduction of the leukocytes, but also lymphocyte decrease and neutrophil increase. Moreover, an elevation in total leukocytes associated with an increase in the humoral immune response was also observed one week after IAR. In this study, the expression of intraspecific aggressiveness in the face of a stressor seemed to activate the immune system and to potentiate the antigen specific humoral response.Key words: intraspecific aggressiveness, leukocytes, humoral immune response. RESUMOA expressão de uma reação agressiva intra-específica diante de um estressor altera a resposta imune em ratos A repercussão sobre a resposta imune da expressão da agressividade intra-específica diante de um estressor foi investigada em ratos. Aos 90 dias de vida, os animais foram divididos em três grupos: grupo-controle (foram realizadas apenas mensurações imunológicas), choque nas patas (FS) (os animais receberam FS individualmente) e grupo resposta agressiva intra-específica (IAR) (os animais receberam FS e apresentaram IAR). Para as medições imunológicas, amostras de sangue foram coletadas imediatamente, 7 e 15 dias após FS ou IAR. O FS reduziu a quantidade total de leucócitos. Contudo, a agressividade foi acompanhada, além da redução do número de leucócitos, por diminuição de linfócitos e aumento de neutrófilos. Além disso, também foi observada elevação no número de leucócitos associada a aumento na resposta imune humoral uma semana após as IAR. Neste estudo, a expressão da agressividade intra-específica diante de um estressor parece ativar o sistema imune e potencializar a resposta humoral antígeno específica.Palavras-chave: agressividade intra-específica, leucócitos, resposta imune humoral.

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Enhancement of Antigen-Specific Humoral and Cell-Mediated Immunity by Electric Footshock Stress in Rats

Cited by 82 publications

References 0 publications

Enhancing versus suppressive effects of stress hormones on skin immune function

Enhancing versus suppressive effects of stress hormones on skin immune function

Enhancing versus Suppressive Effects of Stress on Immune Function: Implications for Immunoprotection and Immunopathology

The expression of an intraspecific aggressive reaction in the face of a stressor agent alters the immune response in rats

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