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Results for “Neuroimmunomodulation”

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At least 577 records · Page 32Linked to original sources
PubMed2005

CD86 and beta2-adrenergic receptor stimulation regulate B-cell activity cooperatively.

IgG1 functions to neutralize and clear foreign antigens, such as extracellular bacteria. Therefore, it is important to understand the multiple mechanisms by which the level of IgG1) is regulated to maintain immune system and host homeostasis. Recent data show that the level of IgG1 produced by a B cell is increased following CD86 and beta2-adrenergic receptor (beta2AR) stimulation, through increased expression of the transcription factor Oct-2 and its coactivator OCA-B (Oct coactivator from B cells), respectively. This finding suggests that signaling pathways that are activated by an immunoreceptor (CD86) and a neuroreceptor (beta2AR) converge to regulate the IgG1 response.

Animals↗
PubMed2004

Neurodegenerative disease and the neuroimmune axis (Alzheimer's and Parkinson's disease, and viral infections).

The appearance of activated immune cells and the accumulation of inflammation-associated proteins are common phenomena associated with neurodegenerative diseases. These inflammatory components of central nervous system (CNS) diseases have most often been described in the context of an immune response to damage and cell loss already occurring in the affected brain area. There has, however, been a renewed interest in how the neuroimmune axis might itself be involved in the etiology of these neurodegenerative diseases, particularly in cases involving slow, chronic, progressive neuropathology. This review addresses immune activation in Alzheimer's, Parkinson's, and brain viral infections that may be causative of, rather than responsive to, the observed neuronal loss in these pathologies.

Alzheimer Disease↗
PubMed2004

Post-receptorial mechanisms underlie functional disregulation of beta2-adrenergic receptors in lymphocytes from Multiple Sclerosis patients.

Increased density of beta2-adrenergic receptors has been demonstrated on peripheral blood mononuclear cells (PBMCs) from Multiple Sclerosis (MS) patients. In this study we found that isoproterenol reduces T-cell proliferation and IFNgamma secretion in PBMCs cultures from healthy controls and IFNbeta-treated but not untreated MS patients. Reduced expression levels of G protein coupled receptor kinase (GRK)2/3 (p < 0.05) and increased isoproterenol-induced cAMP accumulation (p < 0.0001) were found in PBMCs from all MS patients. Dibutyryl cAMP reduced the proliferation of PBMCs from all subgroups but in a slighter manner in untreated MS patients. We conclude that signalling through beta2-adrenergic receptors is chronically up-regulated but functionally uncoupled to immunoregulatory functions of lymphocytes from MS patients. Disregulation downstream the cAMP-associated signalling may underlie such a phenomenon.

Adrenergic beta-Agonists↗
PubMed2004

Chronic electric stimulation of the midbrain ventral tegmental area increases spleen but not blood natural killer cell cytotoxicity in rats.

Previously we found that in conscious, freely behaving rats chronic electric stimulation of the lateral hypothalamus (LH) caused significant augmentation of natural killer cell cytotoxicity (NKCC) and a large granular lymphocyte (LGL) number more pronounced in the spleen than in the peripheral blood. The LH belongs to the so-called "brain reward system", a collection of the central structures whose activation produce positive emotions. The midbrain ventral tegmental area (VTA) is another prominent reward-relevant structure. In the present work, chronic electric stimulation of VTA (constant current 0.1 ms duration cathodal pulses delivered at frequency 50 Hz during 60 min daily session for 14 consecutive days) caused in rats an increase in the spleen but not in the peripheral blood NKCC (chromium release assay) without simultaneous effect on the number of large granular lymphocytes (LGL) (morphological method) and plasma level of prolactin (PRL), growth hormone (GH), corticosterone (COR), and testosterone (TST). This effect was anatomically specific as no influence of analogous thalamic stimulation on immune and endocrine response was found. The results obtained indicate that both reward-related areas VTA and LH enhance the cell-mediated immune response, represented by natural killer cytotoxicity, especially in the spleen. However, the effect pronounced by VTA is weaker than that of LH, possibly due to additional connections of LH with the hormonal and/or autonomic control systems.

Adrenal Cortex Hormones↗
PubMed2004

Transcriptional pattern analysis of adrenergic immunoregulation in mice. Twelve hours norepinephrine treatment alters the expression of a set of genes involved in monocyte activation and leukocyte trafficking.

We investigated in vivo effects of norepinephrine (NE) on the transcription of 200 immunologically relevant genes in the mouse. Balb/c mice were s.c. implanted with NE containing retard tablets. Twelve hours later, splenic mRNA was prepared and hybridized onto cDNA microarrays containing the sequences of the major cytokines, their receptors and all CD-antigens of the mouse. Consistent results were obtained with a set of five genes: in the NE-treated animals four genes (CXCR4, VCAM1, IL-1R2, CD 14) were found 2-8 fold upregulated as compared to sham treated animals, whereas the gene for CCR3 was downregulated (< 0.5 fold). The findings were confirmed using quantitative reverse transcriptase Real Time PCR. These first results prove the usefulness of gene microarray technology towards transcription pattern analysis in neuroimmune interactions. Furthermore, they support the relevance of catecholamines in the regulation of leukocyte migration and the inflammatory response.

Animals↗
PubMed2004

Substance P and neurokinin-1 receptor modulation of HIV.

There is a high incidence of life event stress, depression, and associated symptoms in individuals with HIV infection/AIDS. Psychological and psychiatric symptomatology in individuals with HIV and AIDS may be related to the progression of AIDS disease. The association between depression, anxiety, and stress with HIV disease progression suggests that neurobiologic and neurophysiologic factors have an important role in modulating HIV. The immune effects caused by changes in behavioral state or brain activity are affected, at least in part, through the neuroendocrine-immune pathways. Life stress and depression may be associated with altered blood levels of CNS-released neuropeptides, including substance P (SP). SP is a powerful immunomodulator which is a critical link between the nervous and immune system. We have investigated the role of the neuropeptide SP and its preferred receptor, neurokinin-1, in HIV infection and AIDS. There are compelling data from our laboratories, as well as the findings in the literature, which demonstrate that SP may play an important role in the pathophysiology of neuropsychiatric disorders, including stress and depression in HIV-infected individuals and in the immunopathogenesis of HIV disease. Modulation of SP activity and SP receptor may offer a novel approach to the treatment of psychiatric disorders and to the design of new anti-HIV therapy.

Animals↗
PubMed2005

The immunomodulating neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) suppresses LPS-stimulated TLR4 with IRAK-M in macrophages.

Since alpha-MSH suppresses endotoxin-induced inflammation by innate immunity, it is possible that alpha-MSH can suppress the interface between innate and adaptive immunity mediated by TLR4-stimulated macrophages. Endotoxin-stimulated macrophages treated with alpha-MSH are suppressed in nitric oxide and IL-12p70 production, and cannot enhance antigen-stimulated IFN-gamma production by Th1 cells. In macrophages treated with alpha-MSH, the inhibitory molecule IRAK-M is bound to IRAK-1, the proximal intracellular signal molecule of endotoxin-bound TLR4. These results further demonstrate the dynamic contribution of the nervous system, and the role of alpha-MSH in modulating the innate and adaptive immune interface in an inflammatory response.

Animals↗
PubMed2005

Aging and sympathetic modulation of immune function in Fischer 344 rats: effects of chemical sympathectomy on primary antibody response.

In aged Fischer 344 (F334) rats, sympathetic innervation of the spleen is markedly diminished compared with young rats. To determine if this diminished noradrenergic (NA) innervation maintains a functional connection with the immune system, 3- and 17-month-old male F344 rats were treated with the NA-selective neurotoxin, 6-hydroxydopamine (6-OHDA), to ablate peripheral NA nerve fibers. In sympathectomized rats immunized with keyhole limpet hemocyanin (KLH), a T-dependent protein antigen, anti-KLH IgM, IgG, IgG1, IgG2b antibody titers were increased in young and old rats 14 days after immunization compared to vehicle controls. Furthermore, the number of IgM and IgG anti-KLH antibody-secreting spleen cells was elevated 7 and 14 days post-immunization. These effects were prevented by pretreatment with desipramine, a catecholamine uptake blocker that blocks 6-OHDA uptake and subsequent sympathectomy. Chemical sympathectomy also increased KLH-induced proliferation in vitro by spleen cells from old, but not young animals. Isoproterenol (ISO), a beta-adrenergic receptor agonist, elicited a rise in cAMP in spleen cells from NA-intact young and old rats, but the increase was attenuated in spleen cells from old rats. These results demonstrate that, although NA innervation in the F344 rat spleen is diminished with age, sympathetic signaling of the immune system remains intact. Thus, the SNS can inhibit antibody produced in response to a protein antigen in both young and old F344 rats.

Adrenergic beta-Agonists↗
PubMed2006

Neural-immune interactions: an integrative view of the bidirectional relationship between the brain and immune systems.

This review briefly summarizes a part of the relevant knowledge base of neuroimmunology, with particular emphasis on bidirectional neural-immune interactions. These complex systems interact at multiple levels. Both neuroendocrine (the primary hormonal pathway is hypothalamic-pituitary-adrenal axis) and neuronal (direct sympathetic innervation of the lymphoid organs) pathways are involved in the control of the humoral and cellular immune responses. Although, the recent evidence has been made on immunosuppressive effect of acetylcholine-secreting neurons of the parasympathetic nervous system. The immune system, in turn, influences the central nervous system primarily through cytokines. At the molecular level, neuro- and immune signal molecules (hormones, neurotransmitters, neuropeptides, cytokines) or their receptors are member of the same superfamily which enable the mutual neuroimmune communication. Most extensively studied are cytokine-neuropeptide/neurotransmitter interactions and the subcellular and molecular mechanisms of these interactions. At the system (neuroanatomical) level, advances in neural-immune communication have been made in the role of discrete brain areas related to emotionality. The immunoenhancement, including the antiviral and antitumor cytotoxic activity, related to the "brain reward system", limbic structures and neocortex, offers a new directions for therapy in immune disorders.

Animals↗
PubMed2006

PACAP 38 as a modulator of immune and endocrine responses during LPS-induced acute inflammation in rats.

The effect of PACAP 38 administration on neuroendocrine and immune parameters was examined in rats with LPS-induced peritonitis. Treatment with PACAP 38 alone did not influence the serum level of the cytokines and hormones examined, but significantly decreased immune cell activity. When administered together with LPS, PACAP 38 reversed its effect on immune and humoral parameters, causing a decrease in the serum concentrations of TNFalpha and corticosterone, and an increase in T4 and GH. The majority of PACAP 38 effects disappeared earlier than those previously observed for VIP. PACAP 38 appears to represent a short-lasting modulator of immune and endocrine responses during acute inflammation.

Acute Disease↗
PubMed2006

Neuropeptide Y Y1 receptors mediate morphine-induced reductions of natural killer cell activity.

Morphine suppresses a number of immune parameters, such as natural killer (NK) cell activity and lymphocyte proliferation, by acting through mu-opioid receptors in the central nervous system. Prior studies have implicated the sympathetic nervous system in mediating the immunomodulatory effects of acute morphine treatment. However, the peripheral mechanism whereby morphine inhibits NK cell activity is not fully understood. The aim of the present study was to investigate the role of the sympathetic transmitter neuropeptide Y (NPY) in mediating morphine-induced immune alterations. The results showed that administration of the selective NPY Y1 receptor antagonist BIBP3226 blocked morphine's effect on splenic NK activity but did not attenuate the suppression splenocyte proliferative responses to Con-A or LPS. Furthermore, intravenous NPY administration produced a dose-dependent inhibition of splenic NK activity but did not suppress lymphocyte proliferation. Recent studies from our laboratory have demonstrated that morphine modulates NK activity through a central mechanism that requires the activation of dopamine D1 receptors in the nucleus accumbens. Results from the present study showed that microinjection of the D1 receptor agonist SKF-38393 into the nucleus accumbens shell induced a suppression of NK activity that was reversed by BIBP3226. Collectively, these findings demonstrate that NPY Y1 receptors mediate morphine's suppressive effect on NK activity and further suggest that opioid-induced increases in nucleus accumbens D1 receptor activation inhibit splenic NK activity via NPY released from the sympathetic nervous system.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2006

Neural-endocrine-immune complex in the central modulation of tumorigenesis: facts, assumptions, and hypotheses.

For the precise coordination of systemic functions, the nervous system uses a variety of peripherally and centrally localized receptors, which transmit information from internal and external environments to the central nervous system. Tight interconnections between the immune, nervous, and endocrine systems provide a base for monitoring and consequent modulation of immune system functions by the brain and vice versa. The immune system plays an important role in tumorigenesis. On the basis of rich interconnections between the immune, nervous and endocrine systems, the possibility that the brain may be informed about tumorigenesis is discussed in this review article. Moreover, the eventual modulation of tumorigenesis by central nervous system is also considered. Prospective consequences of the interactions between tumor and brain for diagnosis and therapy of cancer are emphasized.

Animals↗