We studied the effect of acute emotional stress and exogenous IL-1β (5 μg/kg intraperitoneally) on the cytokine profi le of blood serum in Wistar rats with various behavioral characteristics in the open-fi eld test. Blood level of proinfl ammatory cytokine IL-1β decreased in behaviorally passive rats, but increased in active animals after simultaneous immobilization and electrocutaneous stimulation. These changes refl ect the opposite immune responses to a similar stress exposure in rats with different emotional reactivity. Poststress variations in the concentration of circulating IL-1β differed in rats receiving exogenous IL-1β. Blood cytokine concentration decreased in behaviorally active rats, but remained unchanged in passive animals that were exposed to immobilization and electrocutaneous stimulation after pretreatment with IL-1β. Emotional stress and injection of IL-1β had no effect on blood level of an anti-infl ammatory cytokine IL-4 in rats. Our results indicate that rats with various behavioral parameters are characterized by signifi cant differences in the cytokine profi le of blood serum under conditions of emotional stress and treatment with IL-1β. These data illustrate the specifi c functional features of immune mechanisms, which provide an individual resistance of rats to the same stress exposure.A large body of evidence indicates that psychoemotional stress is accompanied by impairment of immune functions in mammals [9]. Immune dysfunction contributes to individual predisposition to stress factors.The pathogenesis of immune dysfunction during emotional stress involves changes in the cytokine profi le. Cytokines are polypeptide transmitters of cellcell interaction playing a regulatory role in normal physiological functions and progression of the defense response to foreign factors and impairment of tissue integrity [1]. Much attention is paid to the superfa mily of IL-1. IL-1β plays a trigger role and induces the cascade of cytokine secretion in the organism. IL-1β is one of the transmitters of the acute phase of the stress response. This cytokine modulates functional activity of the hypothalamic-pituitary-adrenal axis [8]. Our previous studies demonstrated an antistress effect of IL-1β on rats. Intracerebroventricular injection of IL-1β to animals prevents gastric ulceration [3] and involution of the spleen [5] and modulates the oxidative status of the hypothalamus and sensorimotor cortex of the brain under conditions of water-immersion stress [4].
We compared cytokine profile of rat serum and brain structures after immune status modulation by LPS (30 μg/kg intraperitoneally). The content of inflammatory (IL-1α, IL-1β, IL-2, IL-6, IFN-γ, and TNF-α) and anti-inflammatory (IL-4 and IL-10) cytokines in biological samples of animals was measured on days 1 and 7 after antigenic stimulation. LPS administration reduced the levels of both inflammatory and anti-inflammatory cytokines in the peripheral blood of the rats, especially on the 1st day. LPS administration was also accompanied by specific changes in cytokine content in the dorsal hippocampus and anterior cingulate cortex. Antigenic stimulation increased the level of anti-inflammatory cytokines IL-4 and IL-10 in the examined brain tissues, the changes were most pronounced on day 1 after LPS injection. No significant changes in the levels of proinflammatory cytokines in the brain tissue of animals were found at the above terms after LPS injection. Thus, peripheral LPS administration to rats shifts the balance between the inflammatory and anti-inflammatory cytokines in the CNS structures towards the latter.
Acute emotional stress is shown to raise the level of malonic dialdehyde in the hypothalamus of August rats. After intraventricular administration of interleukin-l[3, the malonie dialdehyde level and the activity of antioxidant enzymes tended to rise selectively in the hypothalamus (but not in the sensorimotor cortex) of August, Wistar, and WAG rats. In the presence of this interleukin, acute emotional stress did not cause increases in lipid peroxidation products in the hypothalamus of August rats.
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