Sympathectomy-Induced Immune Changes Are Not Abrogated by the Glucocorticoid Receptor Blocker RU-486

  title={Sympathectomy-Induced Immune Changes Are Not Abrogated by the Glucocorticoid Receptor Blocker RU-486},
  author={Barbara Kruszewska and David L. Felten and Suzanne Y. Stevens and Jan A. Moynihan},
  journal={Brain, Behavior, and Immunity},
Removal of sympathetic noradrenergic input to the immune system by injection of 6-hydroxydopamine (6-OHDA) triggers increases in antigen-specific in vitro splenocyte proliferation and cytokine production in BALB/cJ and C57B1/6J mice. This examines the possible role of glucocorticoids in these previously reported changes. In both strains, chemical sympathectomy triggers an elevation of glucocorticoid levels immediately following injection of 6-OHDA, returning to normal within one to two days. In… 

Chemical Sympathectomy Has No Effect on the Severity of Murine AIDS: Murine AIDS Alone Depletes Norepinephrine Levels in Infected Spleen

It is found that the norepinephrine concentration and content of the spleen were reduced dramatically by the MAIDS infection itself at 3 and 6 weeks after LP-BM5 inoculation, suggesting that the viral infection itself produces a functional sympathectomy in theSpleen, a target of that infection.

The Effects of Chemical Sympathectomy on T-Cell Cytokine Responses Are Not Mediated by Altered Peritoneal Exudate Cell Function or an Inflammatory Response

Evaluated the peritoneal environment into which the protein antigen keyhole limpet hemocyanin is administered and found no evidence of sympathectomy-induced systemic or local splenic inflammatory responses, indicating that an inflammatory response is not likely to be responsible for sympathetic nervous system regulation of immune function.

Neuronally released sympathetic neurotransmitters stimulate splenic interferon-gamma secretion from T cells in early type II collagen-induced arthritis.

It is demonstrated that sympathetic nerves help to increase secretion of IFNgamma and KC, which, at the early stages shortly after the onset of CIA, can contribute to the proinflammatory effect of the sympathetic nervous system.

Suppression of antigen-specific Th2 cell-dependent IgM and IgG1 production following norepinephrine depletion in vivo.

It is suggested that NE stimulation of the beta2AR expressed on B cells is necessary for the maintenance of an optimal primary and secondary Th2 cell-dependent Ab response in vivo.



Alterations in cytokine and antibody production following chemical sympathectomy in two strains of mice.

The results suggest that one function of splenic innervation and transmitter release may be to modulate T helper cytokines, thereby partially regulating immune effector function, and consistent with a model of immune regulation in which removal of sympathetic nervous system input enhances at least some parameters of immune responses.

Neuroimmunomodulation: impairment of humoral immune responsiveness by 6-hydroxydopamine treatment.

6-OHDA treatment has a profound inhibitory effect on the induction of the primary antibody response and immunological memory development, but is without effect on both the IgM and IgG antibody responses to sheep red blood cells (SRBC).

Peripheral Catecholamines Are Involved in the Neuroendocrine and Immune Effects of LPS

Results clearly demonstrate that in vivo, the peripheral sympathetic nervous system participates in the immune and endocrine effects of LPS.

In vivo effects of the antiglucocorticoid RU 486 on glucocorticoid and cytokine responses to Escherichia coli endotoxin

The data suggest that the protective effect of the endogenous glucocorticoid response to acute endotoxemia may result from the down-regulation of a potentially lethal cytokine response and is further associated with significant attenuation of cytokine production.

Corticosteroid‐Mediated Immunoregulation in Man

Observations that activated lymphocytes may be sensitive to the lytic effects of glucocorticoids suggest that under certain situations the elimination of selected subsets of cells may be a relevant mechanism of corticosteroid-mediated immunoregulation in man.

Glucocorticoids accelerate anti-T cell receptor-induced T cell growth.

The regulatory role of glucocorticoids is expanded in cellular immunity, adding a novel effective stimulatory component to their inhibitory properties, and a clear distinction between the enhancing effects of glucOCorticoid on anti-TCR-induced lymphocyte proliferation and their well known inhibitory actions is demonstrated.

The neuroendocrine effects of interleukin-2 treatment.

IL-2 treatment induces the release of neuroendocrine hormones and that a significant increase in hormonal stimulation occurs upon reexposure to IL-2, which is concluded to be a positive effect on stress-related hormones.

Catecholamine influences and sympathetic neural modulation of immune responsiveness.

The importance of the sympathetic nervous system in modulating immune function under normal and disease states is illustrated and the role of chemical sympathectomy in this regard is illustrated.

Contrasting effects of glucocorticoids on the capacity of T cells to produce the growth factors interleukin 2 and interleukin 4

Production of the murine T cell growth factors interleukin (IL)2 and IL 4 are differentially regulated by glucocorticoid (GCS) hormones, implying that GCS hormones function to control the pattern of lymphokines produced by activated T cells.

Differential effects of glucocorticoids on the proliferation of a murine helper and a cytolytic T cell clone in response to IL-2 and IL-4.

The data suggest that the growth effects of IL-2 and IL-4 may be mediated by distinct pathways that are strikingly different in their sensitivity to glucocorticoids, in addition to the regulation of lymphokine-dependent proliferation and the response to glucose appeared very different in helper and cytotoxic cells.