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Results for “Neuroimmunomodulation”

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At least 793 records · Page 44Linked to original sources
PubMed1997

Effect of sciatic denervation on cell-mediated immunity.

Local semiallogenic graft-versus-host (GvH) and host-versus-graft (HvG) reactions were induced in mice whose right hind limbs had been partially denervated surgically. The denervation was performed by removing a 2 mm segment of the sciatic nerve, while sham-operated and non-operated mice served as controls. Eight days after denervation the mice were injected with spleen cells from a 3-month-old C57BL female, or from (C57xCBA)F1 male mice, and the GvH and HvG reactions were evaluated, 7 or 10 days later, by quantitatively estimating the weight (enlargement) of the popliteal lymph-nodes. Significant weight increases of 51% (for the GvH reaction) and 63% (for the HvG reaction) were observed in the denervated mice, when compared to the sham-operated ones. This increased cell-type reactivity in a denervated limbs seems to be related to the immunostimulatory activity of cytokines which are released by cells engaged in repair processes of damaged nerves, as well as related to the reduction of the immunosuppressive effect of noradrenergic innervation in the denervated animals.

Adoptive Transfer↗
PubMedDate not supplied

Morphological and pharmacological evidence for the existence of brain regulatory circuits in the immune response.

Muramyl dipeptide (MDP) has a variety of biological effects including the effect on CNS, such a promotion of sleep, fever, analgesic effect or some behavioural changes and of course a very potent effect on immune system. The latter effect is at least partly mediated through the structure in CNS. With the small electrolytic lesions which were placed in brain from the spinal cord through the brain stem up to the cerebral cortex we have identified a number of structures such as medial frontal cortex (area Cg1-Cg3), subnucleus basomedialis and centralis of amygdala, subnucleus medialis and dorsolateralis of nucleus parabrachialis, lateral part of reticular formation (monoaminergic groups A1-7) and the part of the reticular formation (serotonergic groups B6-B8) which are evidently involved in the immunomodulatory and immunoadjuvant effect of muramyl dipeptide. The results of experiments also suggest that the interaction between neuroendocrine and immune systems might take place on the level of some of above mentioned anatomical structures.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMedDate not supplied

Neuropeptides in the immunomodulation: substance P-induced stimulation of immune response in mice.

The effects of substance P (SP) and its new structural analog EC-1 administered systemically to CBA mice on the immune responsiveness have been examined. Three main findings are presented in this study. First, the principal effect of SP and EC-1 on the immunity is a stimulatory one. It is shown that in the doses of 1, 10 and 100 mkg/kg of the body weight both neuropeptides significantly increased the number of plaque- and rosette-forming cells in the spleen of animals at the peak of the immune reactions. Second, the destruction of the pituitary stalk prevented the immune response stimulation caused by neuropeptides. Third, SP-induced immunostimulation was not observed after combination with the antagonist of the postsynaptic dopamine (DA) D-2 receptors haloperidol (2 mg/kg) suggesting the involvement of the DAergic system in the realization of this effect. Thus, these results demonstrate neurochemical DAergic mechanisms underlying the immunostimulating influence of tachykinins.

Adjuvants, Immunologic↗
PubMed2002

Post-traumatic stress disorder: advances in psychoneuroimmunology.

Exposure to trauma can result in immune dysregulation, and increasing evidence suggests that there are immune alterations associated with post-traumatic stress disorder (PTSD). However, the exact nature of these immune findings in PTSD has not been defined. The study of psychoneuroimmunology in PTSD is relevant not only for understanding the biological underpinnings of this disorder, but also for establishing the nature of the associations between PTSD and other medical and psychiatric illnesses.

Animals↗
PubMed1998

Neuroendocrine and immune system interactions in stress and depression.

Based on the extensive characterization of communication pathways between the nervous system and the immune system, there has been increasing interest in the impact of the nervous system on the development and expression of disorders involving the immune system and the contribution of the immune system to psychiatric disease. A vast literature has documented the impact of various stressors on a wide array of immune partners, and the specific neuroendocrine pathways involved have been elucidated. The impact of cytokines on neuroendocrine function and behavior has also been determined, and the relevance of cytokines to the pathophysiology of depression has become an exciting new research frontier. This article provides a foundation for integrating neuroendocrine-immune interactions into the formulation of neuropsychiatric and immunologic disease.

Depression↗
PubMed1999

Evidence that endogenous thymosin alpha-1 is present in the rat central nervous system.

We have previously reported that administration of Thymosin alpha 1 (T-alpha1) can enhance the level of the Nerve Growth Factor and the distribution of its receptor in the developing Central Nervous System (CNS) of rat. To further explore the role of T-alpha1 and verify its presence in cells of rat CNS, we carried out an immunohistochemical study using a polyclonal antibody against T-alpha1. T-alpha1 immunoreactivity was found mainly in neurons of the hippocampus and spinal cord and in several small cells, resembling glial cells, of specific regions of the brain. Moreover, to study whether cerebral cells were receptive to T-alpha1, we injected iodinated T-alpha1 (125I-T-alpha1) i.c.v.. 125I-T-alpha1 labelled neurons were observed in the hypothalamus and septal nuclei. Our results indicate that specific neuronal populations in the rat CNS are able to express and respond to T-alpha1.

Animals↗
PubMed1998

The influence of neuropeptides, serotonin, and interleukin 1beta on temporomandibular joint pain and inflammation.

PURPOSE: This article describes the possible role of various peptides in producing pain and inflammation in the temporomandibular joint (TMJ). MATERIAL AND METHODS: Current research findings on the spectrophotometric quantification of TMJ synovial fluid for neuropeptide Y (NPY), serotonin (5HT), and interleukin-1beta (IL-1beta) are presented. FINDINGS: NPY was found in high levels in the synovial fluid of arthritic TMJs with resting pain, and serotonin (5-HT) was found in patients with pain perceived on mandibular movement. These pain-related mediators were also associated with restricted mandibular mobility. Interleukin-1beta (IL-1beta) was found to be strongly associated with hyperalgesia over the TMJ as well as resting pain. Anterior open bite as a clinical sign of joint destruction was found to be associated with high levels of NPY and IL-1beta in the synovial fluid. IL-1beta was also related to the radiographic signs of joint destruction. CONCLUSIONS: Interaction between the peripheral nervous system (sensory and sympathetic nerves) and the immune system is probably of importance for the modulation of pain and inflammation in the TMJ, but this subject has to be investigated further with experimental clinical studies.

Animals↗
PubMed2000

Central/peripheral nervous system and immune responses.

Maintenance of health is dependent on numerous regulatory interactions between organ systems. This review discusses interorgan communication between the nervous, endocrine, and immune systems and environmental and genetic influences on this neuroendocrine immune circuitry. Stresses of multiple types, including psychological and exposure to chemicals and infectious agents, may combine to enhance neuroimmunotoxicology. Altered nervous system functions can alter immunity which could result in exacerbation of infections, cancers or other immune-associated problems. Inversely, aberrant immune system activities could lead to pathologies associated with altered nervous activities, such as Alzheimer's disease, chronic fatigue, or multiple sclerosis. The nervous, endocrine and immune circuitry is multi-directional, and a chemical, physical or emotional stress could upset the homeostasis.

Animals↗
PubMed2002

Junctional complexes of the blood-brain barrier: permeability changes in neuroinflammation.

A wide range of central nervous system (CNS) disorders include neuroinflammatory events that perturb blood-brain barrier (BBB) integrity. Mechanisms by which the BBB responds to physiological and pathological stimuli involve signaling systems in the tight and adherens junctions of the cerebral endothelium. In this review, we examine the molecular composition and regulatory mediators that control BBB permeability and assess how these mediators may be dysregulated in stroke, multiple sclerosis, brain tumors, and meningioencephalitis. An understanding of these molecular substrates in BBB regulation may lead to new approaches for enhancing CNS drug delivery and ameliorating brain edema after injury and inflammation.

Adherens Junctions↗
PubMed2000

5-HT-moduline controls serotonergic activity: implication in neuroimmune reciprocal regulation mechanisms.

The serotonergic neurotransmission is known as a neuromodulatory system exerting its activity in the central nervous system (CNS) as well as at the periphery. The anatomical and morphological organization of the system based on a marked centralization of the cellular bodies and the large, almost ubiquitary, presence of axonal projections of the neurons is in good agreement with this modulatory role. Furthermore, a very high number of varicosities located along the axonal branches are capable of releasing serotonin (5-HT). The amine stimulates a number of different specific receptor types which allows 5-HT to exert different activities on its various cellular targets. Among these receptors, the 5-HT1B subtypes play a particular role as they are autoreceptors located on 5-HT neurons terminals and heteroreceptors located on non-serotonergic terminals where they control the release of the neurotransmitter. 5-HT-moduline, an endogenous tetrapeptide, regulates the efficacy of these 5-HT1B receptors, hence, is able to control the serotonergic activity in a synchronous manner for the various varicosities from a single neuron and thus may favour the differential effect of that neuron on distinct cerebral functions. Accordingly, the peptide allows the 'fine tuning' of the cerebral activity by the serotonergic system to elaborate the response given by the brain to a particular stimulus, that is, stress situations. At the periphery, the serotonergic system also appears to possess a regulatory activity via 5-HT1B receptors. In particular, the receptors located on immunocompetent cells control their activity and are themselves regulated by 5-HT-moduline likely originating from adrenal medulla and released after acute stress. The serotonergic system appears to play a major role in the reciprocal signalling existing between the neuronal and the immune system. The participation of 5-HT-moduline is likely in physiological functions as well as in pathological disorders affecting central and peripheral activities.

Animals↗
PubMed1999

Endogenous catecholamine synthesis, metabolism storage, and uptake in human peripheral blood mononuclear cells.

Evidence has been obtained that peripheral blood mononuclear cells contain dopamine, norepinephrine, epinephrine, and their metabolites. Pharmacologic inhibition of tyrosine hydroxylase or monoamine oxidase profoundly affected intracellular catecholamines (CTs) and their metabolites, indicating that these cells are able to synthesize and breakdown CTs. The sensitivity of intracellular CTs to reserpine and the presence of CTs in the extracellular medium suggest that CTs are stored and released. Moreover, the increase of extracellular CTs in the presence of monoamine uptake blockers point to the presence of functional uptake mechanisms. Altogether, these results indicate the existence of a CT lifecycle in human mononuclear cells and warrant further studies to investigate the role of adrenergic autoregulatory mechanisms in modulation of the immune response and in the pathogenesis of diseases involving the immune system.

Adult↗
PubMed2000

Neuroimmune relations in patients with fibromyalgia: a positron emission tomography study.

To study relations between neural and immune activity in patients with chronic pain, we correlated regional cerebral blood flow measured with [(15)O]butanol positron emission tomography to immune function in five patients with fibromyalgia. Partly replicating previous data in healthy volunteers, natural killer cell activity correlated negatively with right hemisphere activity in the secondary somatosensory and motor cortices as well as the thalamus. Moreover, natural killer cell activity was negatively and bilaterally related to activity in the posterior cingulate cortex. Thus, immune parameters were related to activity in brain areas involved in pain perception, emotion, and attention. Implicated from a small study population, these strong neuro-immune associations are discussed in view of recent findings concerning mechanisms and adaptive values in immuno-cortical communication and regulation.

Adult↗
PubMed1998

Melatonin restores and enhances the human type B tonsillar lymphocyte subset in recurrent acute tonsillitis.

Tonsils have a privileged situation in the immune system in that they are in touch with the environment. Melatonin is a hormone that is influenced by the circadian environmental variations of dark-light and is a modulator of the immune system. We have studied a group of thirty five children with recurrent acute tonsillitis that were submitted for tonsillectomy. Tonsillar lymphocyte subsets were determined before and after culture through flow cytometry in a tonsillar mononuclear suspension. After the culture, the lymphocyte subsets of type B suffered a decrease that was restored in the presence of melatonin or phytohemaglutinin, and even increased above the values of the control when the culture was accomplished in the presence of both substances. This process was specific for B cells, no occurrence for T lymphocytes or natural killer cells. Melatonin is found in the crossroads of the interaction of the microorganisms, pollens or inert substances with the tonsillar lymphocytes in the production of the immune defences. Further study is required on tonsillar pathology to explain its physiopathology and its possible therapeutic role.

Acute Disease↗
PubMed1998

Development of systemic lupus erythematosus in mice is associated with alteration of neuropeptide concentrations in inflamed kidneys and immunoregulatory organs.

In the present study we used a well-characterised model of murine lupus, the female NZB/W hybrid, to study the possible involvement of neuropeptides in the pathogenesis of systemic lupus erythematosus (SLE). Analysis of neuropeptides with a possible role in inflammation showed that substance P (SP) calcitonin gene-related peptide (CGRP) and neuropeptide Y (NPY) are present in increased quantities in the inflamed kidneys of SLE mice, confirming their involvement in local inflammation, while there is a general reduction in the peptide concentrations in the lymphoid organs of lupus mice, except for NPY. Our results suggest that the altered neuropeptide concentrations observed in the SLE lymphoid organs may be partly responsible for the altered immune response and contribute to the development of autoimmune diseases.

Animals↗
PubMed2001

NK-1 receptor gene expression is related to pain in chronic pancreatitis.

Recent theories of pathogenesis of pain in chronic pancreatitis (CP) are neuroimmune interactions of intrapancreatic nerves and inflammatory cells and increase in levels of pain neurotransmitters such as substance P (SP). This study analyzed the expression and localization of neurokinin 1 receptor (NK-1R), which binds SP, and its association with pain and inflammation in CP. Pancreatic tissues from 31 patients (22 males, nine females; mean age 45.9+/-9.4 years) with CP were evaluated. Nine normal pancreases (five males, four females; mean age 42.9+/-9.5 years) served as controls. Quantitative PCR was used to determine the NK-1R mRNA expression levels and in situ hybridization and immunohistochemistry were used to localize expression sites of NK-1R mRNA and protein, respectively. We also analyzed whether an association exists between NK-1R mRNA expression and pain and inflammation. In CP samples, in situ hybridization and immunohistochemistry localized NK-1R mRNA expression and protein mainly in the nerves, ganglia, blood vessels, inflammatory cells and occasionally in fibroblasts. In patients with mild to moderate and strong intensity of pain, NK-1R mRNA levels were increased 14- and 30-fold over controls, respectively. There was a significant relationship between NK-1R mRNA levels and intensity of pain (r=0.46, P=0.03), NK-1R mRNA and the frequency of pain (r=0.51, P=0.04), and NK-1 mRNA and duration of pain (r=0.46, P=0.01) in CP patients, but not with the degree of tissue inflammation. NK-1R signaling may be involved in the pain syndrome of CP. The expression of NK-1R in inflammatory cells and blood vessels also points to an interaction of immunoreactive substance P nerves, inflammatory cells and blood vessels, and further supports the existence of a neuroimmune interaction that probably influences the pain syndrome and chronic inflammatory changes so characteristic of CP.

Adult↗
PubMed2002

Focal peripheral nerve injury induces leukocyte trafficking into the central nervous system: potential relationship to neuropathic pain.

The present study was undertaken to determine whether leukocytes are recruited into the spinal cord following a peripheral L5 spinal nerve transection that results in mechanical allodynia (increased tactile sensitivity behavior correlates with neuropathic pain). In rats subjected to bone marrow irradiation, donor-specific major histocompatibility complex (MHC) class I (I1-69) positive peripheral immune cells trafficked to the L5 spinal cord in response to an L5 spinal nerve injury. The number of I1-69 positive cell profiles increased over time and correlated with increased mechanical allodynia. At early time points following injury, I1-69 positive immune cells co-regionalized with the expression of the macrophage marker ED2. At later time points following injury, some of the infiltrating immune cells did not co-regionalize with the macrophage marker ED2. At no time did the infiltrating cells co-regionalize with the neuronal marker (NeuN). Both macrophage-like morphology and T cell-like morphology were observed in the I1-69 positive cellular infiltrate. Conversely, animals that underwent sham surgery demonstrated little mechanical allodynia and a minimal number of infiltrating peripheral immune cells. In a separate group of rats, infiltration of CD3+ T-lymphocytes was confirmed at 14 days post-nerve transection. This study demonstrates trafficking of leukocytes into the lumbar spinal cord at time points that correlate with mechanical allodynia suggesting a role of central neuroinflammation in persistent neuropathic pain.

Animals↗