Stress-Induced Alteration of Polymorphonuclear Leukocyte Function in Rats

Shurin, Michael R.; Kusnecov, Alexander; Hamill, Ellen C.; Kaplan, Sandra S.; Rabin, Bruce S.

doi:10.1006/brbi.1994.1015

Cited by 27 publications

(15 citation statements)

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“…However, they also demonstrated that footshock stress enhanced the phagocytic activity of the neutrophils at the inflammatory site. Similar findings have also been observed in mice exposed to 18 h of restraint stress [55], in humans that have run until exhaustion [56] or that were exposed to moderate exercise (biking) [57], and in rats exposed to repeated restraint stress [58] or a shock-avoidance task [59]. Thus, it is possible that the effects of IS observed in the present experiments may reflect similar changes in phagocytic activity of polymorphonuclear immune cells.…”

Section: Discussionsupporting

confidence: 84%

Acute Stress May Facilitate Recovery from a Subcutaneous Bacterial Challenge

Deak¹,

Nguyen²,

Fleshner

et al. 1999

Neuroimmunomodulation

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The effects of stress on the immune system vary with both the duration and type of stressor. Many studies suggest that stress may compromise an organism’s ability to recover from immune challenge. However, recent findings suggest that stress may actually enhance some aspects of immune function. For example, exposure to a single session (∼2 h) of intermittent inescapable tailshocks (IS) has been shown to activate the acute phase response and increase some aspects of macrophage function. Thus, the following experiments assessed whether IS exposure would alter local inflammation produced by peripheral injection of streptomycin-killed bacteria. Rats (Harlan Sprague Dawley) were exposed to IS (100 1.6-mA, 60 s variable intertrial interval) and injected with Escherichia coli (∼2.5 × 10⁸ CFU s.c. posterior to the shoulder blades). The area of inflammation was measured until the inflammation had completely resolved (typically 7–8 days). When bacteria were administered immediately after IS, rats resolved inflammation significantly faster than did nonstressed rats. Since adrenalectomy did not reduce the effect of IS, it is unlikely that this effect is a result of elevated corticosterone levels. Furthermore, IS does not appear to alter the rat’s ability to sequester bacteria in the subcutaneous space since no swelling of lymph nodes or chronic activation of the hypothalamic-pituitary-adrenal axis was observed.

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Section: Discussionsupporting

confidence: 84%

Acute Stress May Facilitate Recovery from a Subcutaneous Bacterial Challenge

Deak¹,

Nguyen²,

Fleshner

et al. 1999

Neuroimmunomodulation

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“…6 ͉ 2849 33). For example, stress or stress hormones have been shown to enhance cell-mediated (1-3, 34, 35) humoral (36)(37)(38) and innate (39,40) immunity. As summarized in Fig.…”

Section: Dhabhar Et Almentioning

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.

143

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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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“…As demonstrated by several animal and human studies, stress can alter multiple aspects of immune function, including the production of pro-inflammatory cytokines important for wound repair (3)(4)(5)(6)(7)(8). Because neutrophil function is also impaired by stress (9), distressed individuals face additional risks from infection after wounding.…”

Section: Introductionmentioning

confidence: 99%