Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Neuroimmunomodulation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed1999

Proopiomelanocortin and the immune-neuroendocrine connection.

This presentation will cover the history, recent developments in, and implications of the ability of both the immune and neuroendocrine systems to produce POMC. The discovery of POMC in immune cells was one of the events that heralded a molecular understanding of neuroimmunomodulation. This, together with the presence of opiate and ACTH receptors on lymphocytes and macrophages, provided the first biochemical circuit for which the same signal molecules and receptors could be used for intrasystem regulation, as well as bidirectional communication between the immune and neuroendocrine systems. Today we have a quite good understanding of the regulation and processing of POMC in immune cells, as well as the interaction of its product peptides with other cytokines. For instance, IL-1 causes POMC production by immune cells, and the POMC product, alpha-MSH, in turn, acts functionally as an IL-1 antagonist. In the past year, the expression of full-length POMC mRNA has been reported and this solved one of the paradoxes with respect to POMC production, processing, and secretion. We provide data on these developments together with quite startling findings on the physiologic function of POMC peptides in the immune system. Among these are the local antinociceptive effects of immune cell-derived beta-endorphin, altered hematopoiesis in opiate receptor-deficient animals, and the diagnosis of ACTH insensitivity by a deficiency of ACTH receptors on lymphocytes.

Amino Acid Sequence↗
PubMed2000

Gender, neuroendocrine-immune interactions and neuron-glial plasticity. Role of luteinizing hormone-releasing hormone (LHRH).

Signals generated by the hypothalamic-pitutary-gonadal (HPG) axis powerfully modulate immune system function. This article summarizes some aspects of the impact of gender in neuroendocrine immunomodulation. Emphasis is given to the astroglial cell compartment, defined as a key actor in neuroendocrine immune communications. In the brain, the principal hormones of the HPG axis directly interact with astroglial cells. Thus, luteinizing hormone releasing hormone, LHRH, influences hypothalamic astrocyte development and growth, and hypothalamic astrocytes direct LHRH neuron differentiation. Hormonally induced changes in neuron-glial plasticity may dictate major changes in CNS output, and thus actively participate in sex dimorphic immune responses. The impact of gender in neuroimmunomodulation is further underlined by the sex dimorphism in the expression of genes encoding for neuroendocrine hormones and their receptors within the thymus, and by the potent modulation exerted by circulating sex steroids during development and immunization. The central role of glucocorticoids in the interactive communication between neuroendocrine and immune systems, and the impact of gender on hypothalamic-pituitary-adrenocortical (HPA) axis modulation is underscored in transgenic mice expressing a glucocorticoid receptor antisense RNA.

Animals↗
PubMed1999

alpha-MSH and its receptors in regulation of tumor necrosis factor-alpha production by human monocyte/macrophages.

The hypothesis that macrophages contain an autocrine circuit based on melanocortin [ACTH and alpha-melanocyte-stimulating hormone (alpha-MSH)] peptides has major implications for neuroimmunomodulation research and inflammation therapy. To test this hypothesis, cells of the THP-1 human monocyte/macrophage line were stimulated with lipopolysaccharide (LPS) in the presence and absence of alpha-MSH. The inflammatory cytokine tumor necrosis factor (TNF)-alpha was inhibited in relation to alpha-MSH concentration. Similar inhibitory effects on TNF-alpha were observed with ACTH peptides that contain the alpha-MSH amino acid sequence and act on melanocortin receptors. Nuclease protection assays indicated that expression of the human melanocortin-1 receptor subtype (hMC-1R) occurs in THP-1 cells; Southern blots of RT-PCR product revealed that additional subtypes, hMC-3R and hMC-5R, also occur. Incubation of resting macrophages with antibody to hMC-1R increased TNF-alpha concentration; the antibody also markedly reduced the inhibitory influence of alpha-MSH on TNF-alpha in macrophages treated with LPS. These results in cells known to produce alpha-MSH at rest and to increase secretion of the peptide when challenged are consistent with an endogenous regulatory circuit based on melanocortin peptides and their receptors. Targeting of this neuroimmunomodulatory circuit in inflammatory diseases in which myelomonocytic cells are prominent should be beneficial.

Adrenocorticotropic Hormone↗
PubMed2001

Neuroimmune interactions in experimental colitis. An immunoelectron microscopic study.

With its abundance of neurons and immunocytes, the gut is a potentially important site for the study of the interaction between the nervous and immune systems. In this electron microscopic study we have investigated the distribution of substance P (SP)- and vasoactive intestinal polypeptide (VIP)-immunoreactive (IR) nerve terminals and the immunocytes during experimental colitis in the rat. A mild colitis was induced by a luminal enema containing trinitrobenzene sulfonic acid. The most severe inflammation was detected after 2 days and the density and the distribution of the SP- and VIP-IR nerve terminals as well as the immunocompetent cells were studied at that time. Many SP- and VIP-IR nerve terminals were observed in a very close situation to the inflammatory cells. The number of VIP-IR nerve terminals slightly increased in the inflamed area. The gap between the axolemma of the nerve terminals and immunocytes was 20-200 nm. Some lymphocytes and plasma cells were also IR for SP in the inflamed area, whereas no IR immunocytes were observed in the control and in noninflamed area from the same animal. The very close apposition of the SP- and VIP-IR nerve terminals to the inflammatory cells as well as the presence of SP-IR immunocytes in inflamed area support the suggestion that bidirectional neuroimmunomodulation exists in the colon.

Animals↗
PubMed2005

Cholinergic staining of bronchus- associated lymphoid tissue.

The cholinergic staining of human bronchus-associated lymphoid tissue (BALT) was studied in humans. Morsels of the human lung (containing BALT) were harvested, after having obtained the appropriate approvals, during autopsies in 24 human subjects. The samples were stained by means of the enzymatic technique of acetylcholinesterase (AChE) and/or the monoclonal immunohistochemical method of choline acetyltransferase (ChAT). A morphometrical analysis was performed by means of quantitative analysis of images and statistical analyses of the data. AChE and proteins were also measured by biochemical assay. Our results demonstrate that both AChE and ChAT are localized in the BALT of young and old humans. These enzymes undergo age-related changes. The biochemical values of AChE are as follows: 22.3 +/- 2.5 international units in young subjects and 78.5 +/- 1.9 international units in old ones. The morphometrical values of AChE confirm the biochemical ones. The morphometrical data for ChAT are 31.6 +/- 1.4 conventional units in young subjects and 71.2 +/- 1.5 conventional units in old ones. Further results are needed to draw definite conclusions concerning the location and the distribution of these two enzymatic activities in BALT. In our opinion, the presence of AChE and ChAT in BALT can be both 'non-neuronal', with a role in general metabolism, and/or 'neuronal' with a role in neuroimmunomodulation.

Acetylcholine↗
PubMedDate not supplied

Cytokines and fever.

Fever is an excellent example of neuroimmunomodulation in that mediators of immunity initiate a pathway to raise the thermoregulatory set-point, resulting in behavioral and physiological responses that increase body temperature. This rise in temperature is thought to be adaptive, facilitating host defenses. Many cytokines are endogenous mediators of fever (i.e. endogenous pyrogens), including interleukin (IL)-, 1 beta, IL-6 and others. Tumor necrosis factor-alpha may be both an endogenous pyrogen and an endogenous antipyretic or cryogen, depending on the nature of the inflammatory stimuli. Although there is evidence that cytokines within the hypothalamus initiate fever, recent findings indicate that the signal to increase these brain cytokines may be neural (i.e. from peripheral nerves), rather than humoral (i.e. circulating endogenous pyrogen).

Animals↗
PubMed2002

Strong expression of interleukin-1 receptor type I in the rat carotid body.

One of the unsolved key questions in neuroimmunomodulation is how peripheral immune signals are transmitted to the brain. It has been reported that the vagus might play a role in this regard. The underlying mechanism for this immune system-to-brain communication route is related to the binding of cytokines, such as interleukin (IL)-1beta originating from activated immune cells, to their receptors in glomus cells of the vagal paraganglia. The existence of IL-1 receptor type I (IL-1RI) in vagal paraganglia has been proved. On the basis of these studies, a hypothesis is raised that the carotid body, as the largest paraganglion, might play a similar role to that of its abdominal partner. In this study we examined the distribution of IL-1RI in the carotid body by immunohistochemistry (IHC) and Western blotting techniques. The IHC results showed that almost all glomus cells in the carotid body displayed strong IL-1RI immunoreactivity. The IL-1RI-immunoreactive products were localized in the cytoplasm, nucleus, and cell membrane of the glomus cells. The Western blotting results also confirmed the existence of IL-1RI in both membranous and cytoplasmic elements of the carotid body. These results imply that the carotid body not only serves as a chemoreceptor for modulation of cardiorespiratory performance, as traditionally recognized, but also acts as a cytokine chemorereceptor for sensing immune signals.

Animals↗
PubMed2005

Levels of gastrin-releasing peptide and substance P in synovial fluid and serum correlate with levels of cytokines in rheumatoid arthritis.

It is well known that cytokines are highly involved in the disease process of rheumatoid arthritis (RA). Recently, targeting of neuropeptides has been suggested to have potential therapeutic effects in RA. The aim of this study was to investigate possible interrelations between five neuropeptides (bombesin/gastrin-releasing peptide (BN/GRP), substance P (SP), vasoactive intestinal peptide, calcitonin-gene-related peptide, and neuropeptide Y) and the three cytokines tumour necrosis factor (TNF)-alpha, IL-6, and monocyte chemoattractant protein-1 in synovial fluid of patients with RA. We also investigated possible interrelations between these neuropeptides and soluble TNF receptor 1 in serum from RA patients. Synovial fluid and sera were collected and assayed with ELISA or RIA. The most interesting findings were correlations between BN/GRP and SP and the cytokines. Thus, in synovial fluid, the concentrations of BN/GRP and SP grouped together with IL-6, and SP also grouped together with TNF-alpha and monocyte chemoattractant protein-1. BN/GRP and SP concentrations in synovial fluid also grouped together with the erythrocyte sedimentation rate. In the sera, BN/GRP concentrations and soluble TNF receptor 1 concentrations were correlated. These results are of interest because blocking of SP effects has long been discussed in relation to RA treatment and because BN/GRP is known to have trophic and growth-promoting effects and to play a role in inflammation and wound healing. Furthermore, the observations strengthen a suggestion that combination treatment with agents interfering with neuropeptides and cytokines would be efficacious in the treatment of RA. In conclusion, BN/GRP and SP are involved together with cytokines in the neuroimmunomodulation that occurs in the arthritic joint.

Adult↗
PubMed2005

Neuronal, endocrine, and anorexic responses to the T-cell superantigen staphylococcal enterotoxin A: dependence on tumor necrosis factor-alpha.

Staphylococcal enterotoxin A (SEA) is a microbial superantigen that activates T-lymphocytes and induces production of various cytokines, including tumor necrosis factor-alpha (TNFalpha). Previously, it was shown that SEA activates the hypothalamic-pituitary-adrenal axis and augments gustatory neophobic behaviors. In the present study, it was hypothesized that these effects involve neuronal activation in forebrain regions mediating fear and/or anxiety and are dependent on the production of TNFalpha. Male C57BL/6J mice were given intraperitoneal injections of 10 microg of SEA and 5 microg of lipopolysaccharide (LPS) or saline and perfused 2 h later for histochemical determination of brain c-Fos immunoreactivity (IR). The results showed increased c-Fos IR in the paraventricular nucleus, arcuate nucleus, central nucleus of the amygdala, bed nucleus of the stria terminalis, and lateral septum. Challenge of TNF-/- mice with SEA did not produce a significant increase in brain c-Fos IR, although c-Fos was increased after exposure to a psychogenic stressor (i.e., open field). In additional experiments, the elevated corticosterone response to SEA was abrogated in TNF-/- mice and was shown to be corticotropin-releasing hormone dependent. Finally, the augmented reduction in novel food intake after SEA challenge was attenuated in TNF-/- mice as well as in wild-type mice administered antibody to TNFalpha. In conclusion, challenge with SEA recruits brain regions mediating stress and anxiety responses, an effect that requires endogenous TNFalpha. Whether this is indicative of all T-cell superantigens remains to be determined, although it stands in contrast to other models of neuroimmunomodulation (e.g., LPS) that involve multiple cytokine influences.

Animals↗
PubMedDate not supplied

Hemispheric asymmetry in the effects of substantia nigra lesioning on lymphocyte reactivity in mice.

Asymmetry in brain modulation of the immune system has previously been demonstrated at the neocortex level. In these experiments, the possibility of subcortical immunomodulation was investigated. In mice the substantia nigra was lesioned using the neurotoxin 6-hydroxydopamine. Four and six weeks after left or right lesions of the substantia nigra, spleen lymphocyte mitogenesis was slightly depressed or enhanced respectively as compared to sham operated controls. Differences appeared when comparing left and right lesioned groups. However, natural killer cell activity was unaffected by unilateral lesions of the substantia nigra. These results show that asymmetrical brain modulation may occur at the sub-cortical level and suggest that central dopamine is involved in neuroimmunomodulation.

Animals↗
PubMed1993

Brain lateralization and immunomodulation.

The two sides of the brain may be differently involved in the modulation of immune responses as demonstrated by lesional and behavioral approaches in rodents. Lesions of right or left neocortex induced opposite effects on various immune parameters including mitogen-induced lymphoproliferation, interleukin-2 production, macrophage activation or natural killer cell activity. This animal model, useful to elucidate whereby the brain and the immune system can communicate, appears to be suitable for studying the immune perturbations observed during stroke in humans. Brain asymmetry in modulation of immune reactivity may also be demonstrated in intact animal using a behavioral paradigm. The direction of a lateralized motor behavior ie paw preference in a food reaching task, correlated with an asymmetrical brain organization, was shown to be associated with lymphocyte reactivity, natural killer cell activity and auto-antibody production. The association between paw preference and immune reactivity in mice varies according to the immune parameters tested and is a sex-dependent phenomenon in which genetic background may be involved. The experimental models for investigating asymmetrical brain modulation of the immune system should be useful for studying several physiological, pathological and genetic aspects of neuroimmunomodulation.

Brain↗
PubMed1994

Pyrogenic activity of human native and human recombinant interleukins-1 beta: stabilization with albumin enhances the pyrogenic action of recombinant IL-1 beta delivered into the rabbit brain.

The pyrogenic potential of natural and recombinant human IL-1 beta in rabbits was found to be very similar when the substances were given intravenously. Under these conditions, stabilization of rIL-1 beta with human serum albumin (HSA) failed to affect the pyrogenic activity of recombinant IL-1 beta. When the two preparations were administered directly into the PO/AH area of the brain, recombinant IL-1 beta was less pyrogenic than its natural counterpart. This lower pyrogenicity of recombinant IL-1 beta was corrected if the injected material contained HSA, which is known to stabilize in vitro the biological activities of IL-1 beta against slow degradation. The possibility is now considered that the central and peripheral systems for IL-1 inactivation are different. The existence of an intrabrain IL-1 pool is suggested and its significance for neuroimmunomodulation is stressed.

Animals↗
PubMed1989

Neuroscience and occupational therapy: vital connections. 1989 Eleanor Clarke Slagle lecture.

This paper presents the hypothesis that in-depth knowledge of the neurosciences serves as a common denominator that enhances our ability to interpret all aspects of human behavior. Neurobiological information can be used to design research to evaluate our existing treatment philosophy and methodology and to develop new theories and technology. Because occupational therapy addresses widely divergent diagnostic populations, three separate areas along the practice continuum were selected to demonstrate the application of neurobiological concepts: (a) neuroimmunomodulation, (b) organic bases of psychopathology, and (c) traumatic brain injury. Philosophical statements regarding effective methods of teaching neurobiology to occupational therapists are included.

Brain Injuries↗
PubMedDate not supplied

New vistas in immunopsychopharmacology.

The fifties of this century were a time of expansion of psychophysiology, psychopharmacology as well as immunology. But the immune system was considered by several years as completely autonomous, indetifying foreign elements to the host, and clearing them from the body. Selye was the first who put forward the hypothesis that the thymus takes part in stress phenomena and the pituitary-adrenal-endocrine system mediates the relations between stress and immune system. Then many reports on the immunological consequences of behavior were published. Herbert Novera Spector coined the term neuroimmunomodulation (NIM), and used it in the paper published in 1983. First International Workshop on NIM was held in 1985. Advances in research of the past decade brought psychoimmunopharmacology out of the folklore into the science. The perspectives of the development of understanding further details of NIM depend upon application of antisense nucleotides in further experiments, estimation of cytokine level in cerebro-spinal fluid, observations of central effects in patients treated by cytokines, measurements of several immunological, behavioral biochemical and neuroendocrine variables.

Allergy and Immunology↗
PubMed2001

A review on cancer--psychospiritual status interactions.

With the advances in the knowledge of neuroimmunomodulation, a new era of investigations about the chemical basis of the state of mind has been initiated. Both emotions and states of spiritual consciousness may influence immune functions and cancer growth. Stress, anxiety and depressive states are associated with immunosuppression and enhanced frequency of tumors. On the other hand, the states of sexual pleasure and spiritual joy enhance the immune efficacy, by counteracting tumor onset and dissemination. The biochemistry of pleasure and immunostimulation is mainly mediated by pineal indoles and cannabinergic substances, whereas that of stress, anxiety and depression is associated with enhanced production of adrenal steroids, opioids and catecholamines. The sexual repression would allow a progressive immunosuppression through a profound damage in the biochemistry of pleasure. Therefore, a better definition of psychospiritual status-associated neuroimmunochemistry could allow us to improve the immune dysfunction by acting on the same neuroendocrine secretions which are involved in mediating the psychic influence on the immunity, including that against cancer.

Emotions↗
PubMed2002

Can the brain inhibit inflammation generated in the skin? The lesson of gamma-melanocyte-stimulating hormone.

The neuro-immuno-cutaneous-endocrine network is not a simple construct featuring organ systems intimately involved in the bridge between body and mind. Mind-body influences are bi-directional and the skin should be considered an active neuroimmunoendocrine interface, where effector molecules of neuropeptides act as common words used in a dynamic dialogue between brain, immune system and skin. Gamma-melanocyte stimulating hormone (gamma-MSH), one of the principal neuroimmunomodulating peptides, seems to exercise some control on the cutaneous inflammatory process, through a central action mediated by descending anti-inflammatory neural pathways and via local direct influence on inflammatory cells infiltrating the dermis, such as monocytes, macrophages and neutrophils. Gamma-MSH down-regulates the production of proinflammatory cytokines, while the production of the anti-inflammatory cytokine IL-10 is stimulated by gamma-MSH. Finally, gamma-MSH seems to regulate the expression of surface molecules in immunocompetent cells. Thus, further studies may lead to the use of gamma-MSH as an important anti-inflammatory agent in clinical dermatology.

Brain↗
PubMed2001

[The role of neuroimmunoregulation mobilized by enhancing immunologic function via hou hai acupoint antigen injection].

OBJECTIVE: To study the mechanism of neuroimmunoregulation which is triggered by enhancing immunologic function via Hou Hai acupoint antigen injection. METHODS: Immunohistochemical method, immunofluorometric method and RT-PCR were used to examine the different distribution of cytokine immunopositive cells in the brain and expression of cytokines in the spleen of the human IgG sensitized rats received acupoint, subcutaneous and normal rats antigen injections. RESULTS: In the areas of lateral hypothalamic nucleus (LH) and amygdaloid nuclear complex (AA), the distribution of cytokines immunopositive cells with acupoint injection group was significantly increased more than that in the subcutaneous injection group. But the expression of cytokines immunopositive cells both by the acupoint injection and the subcutaneous injection groups reached their peak value in similar time. Double-labelling results showed that the cytokine immunopositive cells were neurons. In the spleens, the expressions of cytokines, IL-2 and IFN, were significantly increased by acupoint injection more than subcutaneous injection. CONCLUSIONS: The time course of neuroimmunoregulation is similar in the immunized rats via both acupoint injection and subcutaneous injection of antigens. But the activity of neuroimmunoregulation is not the same in acupoint and subcutaneous injection groups. Neurons of the LH and AA are the main source of the neuroimmunomodulators. The effect of enhancing immunologic function via Hou Hai acupoint injection is may be more efficient to mobilize the activity of neuroimmunoregulation of immune-associated brain region than modulation of the immune system.

Acupuncture Points↗
PubMed1992

[Cytokines in anorexia nervosa--nutritional or neuroimmunal changes?].

Natural cell-mediated cytotoxicity (CMC), spontaneous release of tumor necrosis factor (TNF-alpha) by mononuclear cells in vitro, and PHA-induced interferon (IFN-gamma) production were examined by standard methods in 14 females with anorexia nervosa (AN) and marked weight loss and in 16 normal matched controls. The results were confirmed by neutralization with monoclonal antibodies. In the anorectic patients there was a significant increase in TNF production (16 +/- 5 vs 4 +/- 3 mu/ml), and depressed CMC (4 +/- 2 vs 10 +/- 3 lytic units per 50/10(6) cells) and IFN-gamma production (172.5 +/- 25 vs 367 +/- 34 mu/ml). Following successful refeeding and nutritional rehabilitation, all values returned to normal. Thus there are changes in cytokines and defective natural cytotoxicity in AN, apparently related to undernutrition and not to neuroimmunomodulation. The increased TNF-release may further suppress food intake and enhance tissue catabolism, suggesting that nutritional rehabilitation should be the earliest therapeutic goal in anorexia nervosa.

Anorexia Nervosa↗