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Results for “Neuroimmunomodulation”

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At least 415 records · Page 23Linked to original sources
PubMed1988

Immune cells and the hypothalamic-pituitary axis in major depression.

To explore changes in immune cell status with changes in the hypothalamic-pituitary (HP) axis in 20 patients with major depression as compared with 20 age-, sex-, and race-matched control subjects, we examined peripheral blood mononuclear cells (PBMC) for total T-cells (T3), total B-cells (B1), two T-cell subsets (T4 and T8), and natural killer cells (NKH1), and we measured the plasma level of cortisol, adrenocorticotropic hormone (ACTH), growth hormone (GH), and prolactin (PRL). The ratio of T4/T8 was increased in the patients. Within the group of control subjects only, increasing age correlated significantly with decreasing plasma PRL. Within the group of patients only, GH positively correlated significantly with T8 and NKH1, as did PRL with NKH1. No between-groups difference was found for T3, B1, T4, T8, NKH1, cortisol, ACTH, GH, or PRL.

Adult↗
PubMed1993

Immunologically induced neuromodulation of guinea pig nodose ganglion neurons.

The influence of specific antigen challenge on the excitability of C-cells in nodose ganglia isolated from actively sensitized guinea pigs was evaluated using intracellular recording techniques. Antigen (ovalbumin) caused a significant depolarization (approximately 8 mV) of the resting membrane potential. Antigen exposure had differing effects on the membrane input impedance; decreasing it in 15 neurons, increasing it in 6 neurons, and having no effect in 8 neurons. About 20% of guinea pig nodose C-cells reveal a long-lasting after-spike hyperpolarization (AHPslow). Antigen challenge reversibly blocked the AHPslow in 4 of 18 neurons studied in 18 ganglia. About 30% of the nodose ganglion neurons display a time- and voltage-dependent inward rectification at membrane potentials more negative than -75 mV. Exposing the ganglion to the sensitizing antigen consistently blocked this response in 8 of 8 neurons. Histological assessment of toluidine blue stained cells revealed that the nodose ganglion contained approximately 100 mast cells. Exposing the ganglion to ovalbumin stimulated mast cell degranulation, as measured by a decrease in number of stained cells, and evoked the release of histamine, PGD2, and immunoreactive peptidoleukotrienes from the tissue. The results support the hypothesis that endogenous inflammatory mediators released during the immediate hypersensitivity (allergic) reactions can modulate the excitability of primary C-fiber afferents. Mechanisms underlying antigen-induced neuromodulation of these neurons include depolarization of the resting membrane potential, changes in membrane resistance, blockade of a time- and voltage-dependent anomalous rectifier, and, in some cells, blockade of the AHPslow.

Action Potentials↗
PubMedDate not supplied

Lymphocyte homing after left or right brain neocortex ablation.

The cerebral neocortex is known to modulate the immune system in an asymmetrical way. Ablations of the left cortex decrease, whereas symmetrical right lesions have no effect, or enhance, T cell functions measured 6-8 weeks after lesioning. However, modifications of immune responses induced by lesions of the brain neocortex could result from a lymphocyte redistribution mediated by glucocorticoids, like that observed during stress. We tested this possibility in the present experiments. Cortical lesions modulated concanavalin A-induced proliferation of both lymph node and spleen lymphocytes in a similar way. Cortical lesions of either side modified neither the lymphocyte distribution of 51Cr-labelled injected lymph node cells, nor the percentage of blood cell subsets. These results show that cortical lesions do not affect lymphocyte homing, and suggest that the brain neocortex immunomodulatory effects are not mediated by glucocorticoids.

Animals↗
PubMed1991

Rise in thymocyte number and thymulin serum level induced by noise.

A high level of noise is known to induce important changes in the immune system. In this work, the effect of sound stress on the circulating level of thymulin and on the cellularity of the thymus gland was studied. The experiments were done in RK mice exposed to a noise level of 100 dB for a period of 1 h. Following the noise exposure, the animals were bled at different times for thymulin titration, or killed in order to evaluate the number of cells and the weight of each thymus. The results indicate that young mice exposed to the stressor stimulus show an increase in serum thymulin titre, and at the same time they show an increment in thymus weight and in thymocyte number compared to control. These results support a new argument in favour of the theory of a central nervous system control on the thymus function.

Age Factors↗
PubMed1991

Splenic immunomodulation with swimming-induced stress in rats.

In order to determine the effects of swimming-induced stress, young male Wistar rats swam for a single session of 2 h duration, or for one 2-h session a day for five consecutive days. The absolute number of splenic mononuclear cells and the in vitro proliferation of mitogen-stimulated (PHA) T lymphocytes were studied. A single swimming session did not significantly diminish the number of splenic mononuclear cells, but it did significantly reduce splenic T-lymphocyte proliferation. This effect on T-lymphocyte proliferation was significantly blocked, in part, by subcutaneous injection of naltrexone before a swimming session. It was not significantly blocked by pre-exercise oral administration of aminoglutethimide. Repeated swimming sessions induced no significant changes in immune parameters. In conclusion, these data suggest that immunosuppression seen with a single swimming-induced stress period may partly be due to endogenous opioids, and that repetition of the swimming session reduced swimming-induced immunomodulation.

Aminoglutethimide↗
PubMed1995

Antibodies against the amino-terminal portion of pro-enkephalin inhibit DNA synthesis in human peripheral mononuclear cells.

Pro-enkephalin (PENK) mRNA and PENK-derived peptides have been reported in lymphocytes, monocytes, and macrophages. Met-enkephalin (ME) and/or synenkephalin (SYN)-containing peptides are produced and released by human peripheral blood lymphocytes (HPBL) activated with phytohemagglutinin (PHA). Furthermore, SYN (PENK 1-70) was cleaved to low-molecular-mass peptides in HPBL. In this work we studied the effect of a mouse monoclonal antibody (mAb) and a rabbit antiserum (pAb) against the C-terminal portion of SYN on DNA synthesis in PHA-activated HPBL. [3H]Thymidine incorporation into HPBL incubated with 0.1 microgram/ml of PHA was tested in the presence of different concentrations of mAb immunoglobulin (Ig) G or different dilutions of pAb. mAb induced a concentration-dependent decrease of [3H]thymidine incorporation into HPBL: 7%, 19%, 28%, and 35% of inhibition was observed with 0.1, 1, 1.5, and 2 micrograms IgG, respectively, reaching values of 65% with 10 micrograms IgG. Similarly, pAb dilutions of 1/500, 1/1000, 1/2000 and 1/4000 inhibited DNA synthesis by 63%, 61%, 43%, and 30%, respectively. The inhibitory effect of mAb and pAb was specific since it was not produced by non-immune mouse IgG or several non-immune rabbit sera and was completely reversed by 1 microM of the synthetic peptide [Tyr63](syn 63-70) synenkephalin. These results suggest that low-molecular-mass SYN-derived peptides released by PHA-activated HPBL may participate in the proliferative response of these cells. This is further evidence that the non-opioid portion of PENK--that is, SYN-derived peptides--may be involved in tissue development.

Amino Acid Sequence↗
PubMed1995

Macrophage recruitment to acutely injured central nervous system is inhibited by a resident factor: a basis for an immune-brain barrier.

Compared to the peripheral nervous system (PNS), the central nervous system (CNS) of mammals has a poor prospect for regeneration. Accumulating evidence suggests that this is due, in part, to differences in how the immune and nervous systems communicate in response to injury. The macrophage is one of the central cells in this communication with the capacity to respond in a variety of ways depending on the conditions of stimulation. After injury, macrophages enter the CNS much later and in fewer numbers than they do the PNS. It is possible that this late and reduced response is not sufficient to modify the CNS environment to one that is conducive to successful regeneration. In the present study we investigated whether the limited macrophage invasion of injured CNS is due to the presence of an endogenous inhibitory factor that is persistent after injury. Using an in vitro migration assay, we show that rat optic nerve (CNS) is deficient in its ability to attract monocytes as compared to rat sciatic nerve (PNS). We further demonstrate that this deficiency is due to the presence of a soluble inhibitory factor in the CNS. This factor may also cause a subsequent effective difference in those macrophages that are recruited, as is shown by morphological data. The brain-resident factor that inhibits macrophage migration may be the physiological basis of an immune-brain barrier underlying the known phenomenon of immune privilege.

Animals↗
PubMed1991

Is interleukin 2 a neuromodulator in the brain?

A bidirectional flow of information exists between the CNS and the neuroendocrine and immune systems, representing an important homeostatic mechanism in the body. Lymphokines and other products of immunocompetent cells seem to play a crucial role in this communication and seem to exert powerful effects on neurones in the brain. In this article, Giuseppe Nisticò and Giovambattista De Sarro describe the central effects following interleukin 2 (IL-2) microinfusion into several areas of the rat brain. The locus coeruleus seems to be the main site in the brain through which IL-2 exerts soporific effects. In addition, the possible transducing mechanisms coupling IL-2 receptor stimulation and the electroencephalogram (EEG) spectrum power responses elicited from the locus coeruleus seem to involve stimulation of specific receptors coupled to adenylate cyclase through a Gi protein.

Animals↗
PubMed1991

Genetic variation in the stress response: susceptibility to experimental allergic encephalomyelitis and implications for human inflammatory disease.

Glucocorticoids that are released from the adrenal glands in response to stress can have profound effects on the immune system. Here, Don Mason illustrates how genetic variation in the magnitude of such a response can determine susceptibility to an experimental autoimmune disease in rats and discusses the implications for susceptibility to inflammatory diseases in humans. He also addresses the possible long-term effects of glucocorticoids on the balance between the cell-mediated and the humoral aspects of immunity and how this balance may influence the temporal development of an immune reaction.

Animals↗
PubMed1993

Interleukin 1 receptors in the brain and endocrine tissues.

Immune activation is often accompanied by profound alterations in neurological and endocrine function, such as fever, increased somnolence, decreased appetite, activation of the hypothalamic-pituitary-adrenal axis, and suppression of the hypothalamic-pituitary-gonadal and hypothalamic-pituitary-thyroid axes. These well-recognized systemic responses to injury and infection have been attributed to circulating pro-inflammatory cytokines, the best characterized of which is interleukin 1 (IL-1). Here Emmett Cunningham and Errol De Souza discuss the mechanisms by which blood-borne IL-1 might affect such changes in the nervous and neuroendocrine systems.

Animals↗
PubMed1995

Unraveling the neuroimmune mechanisms for the HIV-1-associated cognitive/motor complex.

Infection of the brain with human immunodeficiency virus 1 (HIV-1) often leads to the devastating loss of mental faculties. Surprisingly, HIV-1 elicits such brain dysfunction without significantly infecting neurons, astrocytes and oligodendroglia. The target for HIV-1 in the brain is the macrophage, which usually functions as a phagocytic, antigen-presenting and immune-regulatory cell. How can these cells produce such serious cognitive and motor brain impairments? Here, Hans Nottet and Howard Gendelman propose that HIV-1 penetrates the blood-brain barrier inside differentiating macrophages, which become immune activated once inside the brain, and secrete high levels of neurotoxins. Chronic, subclinical disease results by astrocyte regulation of macrophage effector functions. Ultimately, endogenous control mechanisms break down, leading to motor and mental impairments in some affected subjects.

AIDS Dementia Complex↗
PubMed1989

Sympathetic control of specific and non-specific immune response.

Following antigenic stimulation with specific (alloantigen) and non-specific (sheep red blood cells (SRBC) and lipopolysaccharide (LPS] antigens the expression of beta-adrenergic receptors and the interference of immune sera IgG, on uterine smooth muscle beta-adrenoceptor-specific ligands were studied. The binding of alloimmune IgG to beta-adrenoceptors appeared to be specific, because immunization with SRBC and LPS did not induce anti-beta-adrenoceptors antibodies. On the contrary, the decrease in beta-adrenergic receptor expression was observed even with alloantigens and with the conventional antigenic challenge, suggesting that this phenomenon could be a non-specific immunoregulatory mechanism.

Animals↗
PubMed1991

Effects on immune responses in rats after neuromanipulation with capsaicin.

The effect of capsaicin treatment on the immune response, assessed as antibody formation in vivo and in vitro, was studied in ovalbumin (OA)-immunized rates. Rats were treated with capsaicin at 1-2 days of life or at adult age, before or after immunization. The levels of IgA, IgE and IgG antibodies as well as immunoglobulins were measured in serum and supernatants from cultured lymph node cells, spleen cells and peripheral blood lymphocytes. Capsaicin treatment affected the antibody levels depending on the timing of capsaicin treatment in relation to immunization. Different effects of capsaicin treatment were also observed on the different immunoglobulin isotypes. One of the most striking effects by capsaicin treatment was the reduction of IgA and IgG synthesis in cultured lymphoid cells from aerosol immunized animals treated with capsaicin after immunization. In contrast, in vivo the level of total serum IgA was increased in similarly treated animals. In this study we show that capsaicin treatment, which is known to decrease the levels of neuropeptides of sensory origin, has a time-dependent effect on both antibody levels in vivo as well as the formation of immunoglobulin in vitro. Although the mechanisms responsible for this are not obvious, we conclude a link between depletion of neuropeptides in sensory nerves and the antibody synthesis.

Animals↗