The Effect of Stress on the Migration of Leucocytes Into the Peritoneal Cavity of Rats Following Injection of an Inflammatory Agent

Bassett, J.R.; Tait, Noel

doi:10.1038/icb.1981.58

Cited by 15 publications

(3 citation statements)

References 5 publications

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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: 72%

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: 72%

Acute Stress May Facilitate Recovery from a Subcutaneous Bacterial Challenge

Deak¹,

Nguyen²,

Fleshner

et al. 1999

Neuroimmunomodulation

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“…Stress reduces migration of leukocytes into the site of inflammation [32]. Moreover corticosteroids can decrease the permeability of the blood-brain barrier [331.…”

Section: Discussionmentioning

confidence: 99%

Suppression of Acute Experimental Allergic Encephalomyelitis by the Synthetic Sex Hormone 17-Alpha-Ethinylestradiol: An Immunological Study in the Lewis Rat

Trooster

Teelken

Kampinga

et al. 1993

Int Arch Allergy Immunol

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Induction of experimental allergic encephalomyelitis (EAE) in female Lewis rats led to the well-known clinical symptoms and histological signs. Treatment with the synthetic estrogen 17-α-ethinylestradiol (EE) from day ––4 before induction until day 21 after induction resulted in partial suppression of these signs and symptoms. Analysis of the peripheral blood leukocyte (sub)populations in these treated animals indicated some remarkable changes. However, these changes were also observed without EE treatment. EE treatment of EAE rats resulted in a significant decrease of the relative weights of both thymus and spleen, which changes however were not reflected in the peripheral blood. Apparently the effects of EE treatment on EAE in the present experiments indicate an action locally at the site of the EAE lesion and do not seem to be mediated by gross changes in the levels of peripheral blood leukocytes.

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“…Several researchers have shown the anti-inflammatory effects of acute stress [29][30][31] . However, many studies using animal models revealed that different types of acute stress are accompanied by a reduction in immune system activity [32,33] .…”

Section: Discussionmentioning

confidence: 99%

Acute and Chronic Stress and the Inflammatory Response in Hyperprolactinemic Rats

Ochoa-Amaya¹,

Malucelli²,

Cruz‐Casallas³

et al. 2010

Neuroimmunomodulation

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Background/Aim: Prolactin (PRL), a hormone produced by the pituitary gland, has multiple physiological functions, including immunoregulation. PRL can also be secreted in response to stressful stimuli. During stress, PRL has been suggested to oppose the immunosuppressive effects of inflammatory mediators. Therefore, the aim of the present study was to analyze the effects of short- and long-term hyperprolactinemia on the inflammatory response in rats subjected to acute or chronic cold stress. Methods: Inflammatory edema was induced by carrageenan in male rats, and hyperprolactinemia was induced by injections of the dopamine receptor antagonist domperidone. The volume of inflammatory edema was measured by plethysmography after carrageenan injection. Additionally, the effects of hyperprolactinemia on body weight and serum corticosterone levels were evaluated. Results and Conclusion: Five days of domperidone-induced hyperprolactinemia increased the volume of inflammatory edema. No differences in serum corticosterone levels were observed between groups. No significant differences were found among 30 days domperidone-induced hyperprolactinemic animals subjected to acute stress and the inflammatory response observed in chronic hyperprolactinemic animals subjected to chronic stress. The results suggest that short-term hyperprolactinemia has pro-inflammatory effects. Because such an effect was not observed in long-term hyperprolactinemic animals, PRL-induced tolerance seems likely. We suggest that short-term hyperprolactinemia may act as a protective factor in rats subjected to acute stress. These data suggest that hyperprolactinemia and stress interact differentially according to the time period.

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The Effect of Stress on the Migration of Leucocytes Into the Peritoneal Cavity of Rats Following Injection of an Inflammatory Agent

Cited by 15 publications

References 5 publications

Acute Stress May Facilitate Recovery from a Subcutaneous Bacterial Challenge

Acute Stress May Facilitate Recovery from a Subcutaneous Bacterial Challenge

Suppression of Acute Experimental Allergic Encephalomyelitis by the Synthetic Sex Hormone 17-Alpha-Ethinylestradiol: An Immunological Study in the Lewis Rat

Acute and Chronic Stress and the Inflammatory Response in Hyperprolactinemic Rats

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