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Results for “Neuroimmunomodulation”

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At least 109 records · Page 6Linked to original sources
PubMed2000

Marshaling the Anti-Inflammatory Influence of the Neuroimmunomodulator alpha-MSH.

Inflammation in peripheral tissues should benefit from a novel focus on descending neuroimmunomodulatory anti-inflammatory influences stemming from CNS receptors for the peptide alpha-MSH. Because activation of glial and peripheral cell receptors modulates inflammatory activity, alpha-MSH peptides may aid treatment of a variety of CNS and peripheral inflammatory disorders. Activation of melanocortin receptors should thus promote control of inflammatory diseases.

Journal Article↗
PubMed1988

Neuroimmunomodulation: potentiation of delayed hypersensitivity and antibody production by chronic electrical stimulation of the rat brain.

This study deals with the structural and functional correlates of the immunoneuroendocrine interconnections, and explores the effects of localized brain stimulation on immune response. Bilateral symmetrical electrodes were placed in the dorsomedial nucleus, ventromedial nucleus and posterior area of the hypothalamus, and in the sensorimotor cerebral cortex of the rat brain. Electrical stimulations were applied for 39 consecutive days, 10 days before and 29 days after single immunization. In sham-stimulated rats, electrodes were lowered into the hypothalamic areas and sensorimotor cortex without passing any current. Animals with electrodes were divided post mortem into groups according to the histological location of the electrode tips. Intact rats served as additional controls. All animals were immunized with bovine serum albumin in complete Freund's adjuvant and tested for immune reactions 7, 14, 21, and 28 days after immunization. The most significant finding was the potentiated delayed skin hypersensitivity and, to a lesser extent, antibody production to bovine serum albumin in rats with stimulated dorsomedial hypothalamus and sensorimotor cortex. On days 21 and 28, skin reactions increased in rats with stimulated posterior hypothalamus. These immune effects could not be obtained when the stimulation was applied to the hypothalamic ventromedial nucleus. Several pathways of the immunoneuroendocrine interplay are suggested.

Animals↗
PubMed1988

Participation of serotoninergic system in neuroimmunomodulation: intraimmune mechanisms and the pathways providing an inhibitory effect.

Exogenous serotonin administration as well as its precursor 5-oxytryptophan, blockade of the ferment inactivation by MAO inhibition, impairment of the monoamine binding, in other words, all the ways of elevation of active serotonin level, result in the inhibition of the immune response. On the contrary, exclusion of the serotoninergic system by the nuclei raphe lesion and the blockade of the synthesis ferments by p-chlorphenylalanine and p-chloramphetamine stimulates it. The present analysis permits us to conclude that the nuclei raphe serotoninergic system provides an inhibitory mechanism of the immune response modulation, that is realized via the hypothalamus-hypophysis-adrenals axis. Immune response modulation by the extraimmune control system is possible only be means of the mechanisms that are present in the immunocompetent system. Investigation of the cellular basis of physiological mechanisms of serotoninergic regulation of the immune process made it possible to determine alterations in the correlation of functionally different cell populations in animals with elevated serotonin level. An inhibitory action which serotonin produces upon the immunogenesis, is based on the attenuation of suppressor cell function, an earlier than under the normal immune response development emergence of suppressor in the population of cell organs, and their longer presence, that is to some extent connected with the redistribution of cell populations in the immunocompetent organs. After serotonin administration only the antigen-nonspecific immunosuppression is activated. In evolutionary terms the mechanisms of nonspecific suppression have been formed earlier than those of specific ones (Calkins & Stutman, 1978; Mijawaki, Seki, Kubo & Tanigushi, 1979). It is quite reasonable that extraimmune modulation, and psychoneuroimmunomodulation by monoamine systems in particular, can be performed by means of this ancient antigen-nonspecific mechanism of the immune response regulation. In this case, the modulation of immunological reactivity should correspond to these endogenous and environmental influences. Thus, activation of the nonspecific suppression induced through the serotoninergic system can be considered as the universal mechanism which on the one hand completes control of the immune homeostasis and on the other may be the precondition of the development of pathological states caused by the reduction of immunological status.

Adrenalectomy↗
PubMed1986

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

Previous studies from this laboratory and others show that perturbations of the central nervous system modulate immune function. In addition, reports from several investigators indicate that depletion of the neurotransmitter norepinephrine (NE) in peripheral nerves by injecting the neurotoxin 6-hydroxydopamine (6-OHDA), can enhance or suppress the antibody response. However, immunocompetence following brain depletion of catecholamines has not been investigated. In this study, we investigated the effects of injecting 6-OHDA into the cisterna magna of male CBA/J mice, and determined the effects of this treatment on both the IgM and IgG antibody responses to sheep red blood cells (SRBC). Both responses are suppressed compared to saline-injected control or normal animals. Animals treated with 6-OHDA have decreased levels of NE in the midbrain, pons-medulla and hypothalamus, while dopamine levels did not change in these brain regions but was decreased in the striatum. The percentage of splenic T cells and B cells was not affected by 6-OHDA treatment. Although there is a marked increase in plasma corticosterone levels in 6-OHDA-treated mice, saline-injected control animals have equivalent increases in plasma corticosterone without concomitant impairment of the immune response. Thus, the decline in immune responsiveness following 6-OHDA treatment does not result from corticosterone-induced immunosuppression. Analysis of the kinetics of the primary IgG response following 6-OHDA treatment indicates that the magnitude, but not the kinetics, of the response decreases. Experiments to determine the effects of 6-OHDA on the afferent and efferent phrases of the response demonstrate that it is effective only when administered prior to immunization, and thus must inhibit early events involved in the initiation of the response. Additional experiments show that mice can be immunized 2 weeks following brain catecholamines depletion and still exhibit a decreased antibody response. However, the response returns to normal levels if immunization is delayed 4 weeks after injection. Further experiments demonstrated that 6-OHDA treatment has no effect on the secondary antibody response, but does inhibit the development of immunological memory. Collectively, these results indicate that 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 the secondary antibody response. The data further substantiate the existence of a link between the brain and the immune response.

Animals↗
PubMed1987

[Neuroimmunomodulation of the immune response by the endocrine system: effect of luteinizing hormone (LH) on the proliferative response of lymphocytes].

Proliferative response of splenic lymphocytes from adult (2 months old) male mice to human luteotrophic hormone (hLH) was studied in vitro. hLH induced lymphoblastic transformation at a concentration of 0.1 micrograms/ml or higher. This hormone potentiated the mitogen activities of concanavalin A (ConA) and phytohemagglutinin (PHA) for T cells and of pokweed mitogen for B and T cells. The data suggest that peripherally circulating LH may regulate a certain function of lymphoid cells.

Animals↗
PubMed1987

Neuroimmunomodulation with enkephalins: in vitro enhancement of natural killer cell activity in peripheral blood lymphocytes from cancer patients.

To initiate investigations into the effects of enkephalins on immune function in cancer patients, the effect of methionine-enkephalin and leucine-enkephalin on natural killer (NK) cell activity in isolated peripheral blood lymphocytes from cancer patients was investigated. Incubation of lymphocytes with either enkephalin resulted in significant increases in NK cell activity. At effector:target cell ratios of 100:1, 33:1 and 11:1 leucine-enkephalin significantly (p less than 0.05) enhanced NK activity at dilutions of 10(-6), 10(-8), 10(-10), and 10(-14) mg/ml. Similar results were obtained with methionine-enkephalin with the exception that the 10(-6) dilution gave insignificant changes at both the 33:1 and 11:1 cell ratios. The results indicate a difference in dose response to both enkephalins between lymphocytes from cancer patients and normal volunteers.

Adjuvants, Immunologic↗