Restraint stress-induced elevations in plasma corticosterone and β-endorphin are not accompanied by alterations in immune function

Flores, Christopher M.; Hernandez, Monica C.; Hargreaves, Kenneth M.; Bayer, Barbara

doi:10.1016/0165-5728(90)90015-f

Cited by 54 publications

(16 citation statements)

References 16 publications

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“…Although stressful events are known to induce alterations of immunity [1,6,8,30,31], we found that ConA-induced lymphocyte proliferation was similar in all groups. This lack of stress effect on pro liferation can be explained by the fact that exposure of lymphocytes to glucocorticoids is required to be longer than 1 h for the steroid to exert an immunosuppressive action [16] and, in our study, splenocytes were removed from donors 1 h following stressor application. Another possibility could be that stress-released immunostimulatory hormones, such as prolactin, either from the neu roendocrine system or by activated lymphocytes, may have counteracted a possible effect of increased cortico sterone levels [21].…”

Section: Discussionmentioning

confidence: 96%

“…In addition to studies reporting stress-induced reductions on immunity [5][6][7], recent lines of evidence indicate that, under several cir cumstances, stress can lead to an enhancement of certain immune responses [8][9][10] and also that acute stres-induced immunosuppression may return to normal values [11][12][13] or even result in immunoenhancement [2,14,15] with repeated exposure to stress. Additionally, evidence also exists of stressful situations involving activation of neuroendocrine activity which is not accompanied by alterations in the immune response [16].…”

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confidence: 99%

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Mutually Antagonistic Effects of Corticosterone and Prolactin on Rat Lymphocyte Proliferation

Sandi

Cambronero²,

Borrell³

et al. 1992

Neuroendocrinology

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The present study was designed to evaluate the immunological outcome resulting from experimental conditions involving different corticosterone and prolactin ratios in rats. One set of experiments was conducted to assess the effects of prolactin and corticosterone on the in vitro mitogen-induced proliferation of spleen lymphocytes from animals previously submitted to the manipulation of their glucocorticoid status throughout adrenalectomy (ADX) and/or exposure to acute stress. The results indicated that prolactin (5 × 10^–9 M) induced a significant increase in concanavalin A- (ConA) induced proliferation of splenocytes only from ADX-control, unstressed, rats. However, a lower dose of prolactin (10^–9M) failed to influence lymphoproliferation. Corticosterone (2 × 10^–8 and 10^–7M) induced a dose-dependent reduction in lymphocyte proliferation in all experimental groups. Further experiments were conducted to study the relative potency of prolactin to antagonize the in vitro corticosterone-induced suppression of ConA-stimulated lymphocytes. The results showed, on the one hand, that higher doses of prolactin (10^–8 and 5 × 10^–8M) were effective in stimulating ConA-induced lymphocyte proliferation in control, undisturbed, rats. They also showed that when prolactin and corticosterone are simultaneously added to the cultures, the immunostimulatory effect induced by a dose of 10^–8M of prolactin can either predominate over a weak suppressive action of corticosterone (2 × 10^–8M) or totally antagonize to normal values a marked immunosuppression induced by a higher dose of corticosterone (10^–7M). These data support the view that different ratios between prolactin and corticosterone concentrations can result in differential immunological outcome. They also suggest that under conditions involving high levels of prolactin, the immunostimulatory properties of prolactin on T cell function may predominate over the immunosuppressive effects of corticosterone.

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Section: Discussionmentioning

confidence: 96%

mentioning

confidence: 99%

Mutually Antagonistic Effects of Corticosterone and Prolactin on Rat Lymphocyte Proliferation

Sandi

Cambronero²,

Borrell³

et al. 1992

Neuroendocrinology

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“…The present study used a common paradigm to induce mild to moderate psychological stress [34]. Although animals may show gradual habituation to daily restraint in physiological measures, it nevertheless causes chronically diminished motor deficits [19,22,35].…”

Section: Discussionmentioning

confidence: 99%

Synergistic effects of age and stress in a rodent model of stroke

Merrett

Kirkland

Metz

2010

Behavioural Brain Research

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Ageing and stress represent critical influences on stroke risk and outcome. These variables are intricately linked, as ageing is frequently associated with gradual dysregulation of the hypothalamic-pituitary-adrenal axis. This study determined the effects of stress on motor function in aged rats, and explored possible interactions of age and stress on motor recovery following stroke in a rat model. Young adult (4 months) and aged (18 months) male Wistar rats were tested in skilled and non-skilled movement before and after focal ischemia in motor cortex. One group of each age received restraint stress starting seven days pre-lesion until three weeks post-lesion. Aged rats were less mobile and stress further diminished their overall exploratory activity. Aged rats were also less proficient in motor skill acquisition and slower to improve after lesion. Stress diminished post-lesion improvement and prevented recovery of endpoint measures. The larger functional loss in aged rats vs. young rats was accompanied by greater damage of cortical tissue and persistent elevations in corticosterone levels. The behavioural and physiological measures suggest limited ability of aged animals to adapt to chronic stress. These findings show that age or stress alone can modulate motor performance but may have greater influence by synergistically affecting stroke recovery.

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“…When stress is chronic and the individual fails to cope with it, prolonged activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system may cause mental health problems such as anxiety and depression [21,22] , as well as physiological troubles such as alterations in immune competence [23] . Restraint stress, which is a model of physical stress [24] , has been shown to affect a number of immunological functions [25][26][27][28][29] . Several reports have evaluated the impact of stress on the immune system.…”

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confidence: 99%

The Impact of High Anxiety Level on Cellular and Humoral Immunity in Mice

Rammal

Bouayed

Falla³

et al. 2009

Neuroimmunomodulation

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Background/Aims: In the present study, we aimed to examine whether a high anxiety level affects various parameters of immunity in mice. Methods: We used the behavioral light/dark choice test to evaluate whether high anxiety has an impact on various parameters of cellular (granulocytes, monocytes, total lymphocytes, TCD4⁺, TCD8⁺ and NK numbers) and humoral (IgA, E and G concentrations) immunity. Secondly, we investigated whether the cellular and humoral immune systems of mice with contrasting levels of anxiety responded differently to stressors (such as physical restraint) by monitoring blood markers of the both types of immunity. Results: High levels of anxiety inhibited part of the cellular and humoral immune systems by significantly decreasing total lymphocytes numbers (including TCD4⁺ and TCD8⁺) and immunoglobulin (A and E) concentrations. However, no significant changes in the number of granulocytes, monocytes or NK cells were observed. As a consequence, overall, our results suggest that high anxiety led to a decrease in the efficiency of the immune system of anxious mice. On the other hand, our findings also showed that restraint stress (acute and subacute) produced the same immunological profile as high anxiety in mice. This was independent of the animals’ anxiety status. At the same time, we observed that restraint stress produced significant increases in the levels of granulocytes and monocytes. Conclusions: High anxiety and restraint stress exerted adverse effects on cellular and humoral immunity in mice. While the effect of restraint stress was independent of the anxiety levels in mice, this stress led to an aggravation of the immune response from the high degree of anxiety. Therefore, anxious subjects could be more vulnerable to infections and inflammation, particularly when they are exposed to stressful situations.

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Restraint stress-induced elevations in plasma corticosterone and β-endorphin are not accompanied by alterations in immune function

Cited by 54 publications

References 16 publications

Mutually Antagonistic Effects of Corticosterone and Prolactin on Rat Lymphocyte Proliferation

Mutually Antagonistic Effects of Corticosterone and Prolactin on Rat Lymphocyte Proliferation

Synergistic effects of age and stress in a rodent model of stroke

The Impact of High Anxiety Level on Cellular and Humoral Immunity in Mice

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