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      Splenic Norepinephrine and Serum Corticosterone Level Fluctuations Associated with Bacteria-Induced Stress

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          Corticosterone (CORT) and norepinephrine (NE), two effector molecules of the hypothalamic-pituitary-adrenal (HPA) and the sympathetic-lymphoid (SL) axes, respectively, differentially influence murine host resistance to Listeria monocytogenes (LM). Serum CORT and splenic NE levels early (≤24 h) after infection correlated positively with host resistance, as long as the LM burden did not exceed approximately 10<sup>6</sup> cfu LM per spleen. As previously reported, mice with right-circling preference (R-mice) have significantly greater host resistance to LM than those with left-circling preference (L-mice) and early after infection, R-mice had significantly higher serum CORT levels than L-mice. However, rapid pathogenesis with a high bacterial burden induced high activation of the HPA and SL axes, which prevented observable differences in the defense against LM, especially later in infection. With the high bacterial inoculum (10<sup>5</sup> LM), the splenic NE levels significantly increased, but no differences among R- and L-mice were discernible. We suggest that endogenous asymmetry of neuroimmune circuits contributes to differential host resistance, but the level of stress (bacterial inoculum) is critical. With regard to the neuroendocrine factors assessed, CORT, but not NE, levels significantly correlated with the enhanced defenses of R-mice in comparison to L-mice. The differential host resistance based on brain laterality seems to be more a function of the HPA axis and possibly other CNS effects on peripheral immunity than neurotransmitter release by the sympathetic innervation of the spleen.

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          Most cited references 13

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          Enhancing versus suppressive effects of stress hormones on skin immune function.

          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 stress-induced 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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            Dopamine  -hydroxylase deficiency impairs cellular immunity

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              Sympathetic nervous system plays a major role in acute cold/restraint stress inhibition of host resistance to Listeria monocytogenes.

               L. Cao (2002)
              BALB/c mice exposed to acute cold/restraint stress (ACRS) had significantly lower host resistance to Listeria monocytogenes (LM) than controls. The stress hormones corticosterone (CORT) and norepinephrine (NE), which are known to modulate immune responses, were evaluated as the cause of the decline in immune defense. The involvement of CORT and NE was investigated by pretreating mice with the CORT synthesis inhibitor metyrapone and the chemical sympathectomy drug 6-hydroxydopamine (6-OHDA), respectively. LM burdens in spleen and liver were determined three days post-infection. 6-OHDA significantly decreased the LM burden in both control and stressed animals. 6-OHDA also completely blocked the stress effects observed in spleens while only partially affecting the liver. The 6-OHDA-uptake inhibitor desipramine aided confirmation that peripheral sympathetic adrenergic nerves and NE depletion, rather than the direct action of 6-OHDA, were responsible for the decreased susceptibility to LM. The results suggest that the peripheral sympathetic nervous system (SNS) postganglionic neurotransmitter NE plays a major role in LM host resistance and has significant tissue-dependent effects after ACRS. In contrast, metyrapone-treated animals had further decreased host resistance to LM, suggesting a potential protective effect of CORT after ACRS. Altogether, the results suggest that stress hormones play an important role in stress-modulated host resistance and that NE is the major hormone involved in ACRS-induced suppression of host resistance.

                Author and article information

                S. Karger AG
                August 2004
                20 August 2004
                : 11
                : 5
                : 323-331
                Laboratory of Clinical and Experimental Endocrinology and Immunology, Wadsworth Center, New York State Department of Health, Albany, N.Y., USA
                79413 Neuroimmunomodulation 2004;11:323–331
                © 2004 S. Karger AG, Basel

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                Page count
                Figures: 6, References: 48, Pages: 9
                Original Paper


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