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PubMed1995

Corticotropin-releasing hormone involvement in stressor-induced alterations in sleep and in the regulation of waking.

Sleep responds to a variety of stressors, but the precise mechanisms whereby these alterations occur are not known. Ample evidence, however, testifies to corticotropin-releasing hormone (CRH) being uniquely situated to contribute to stressor-induced alterations in sleep. Behavioral responses to most stressors include periods of increased arousal and waking, regardless of whether the stressor is psychological in nature or results in physical insult. Furthermore, a large body of evidence suggests that CRH may also contribute to the regulation and maintenance of physiological waking. In this paper we hypothesize that CRH mediates waking, particularly after periods of exposure to acute stressors. The complex interactions of multiple systems determine the behavioral response to a particular stressor. As such, many factors determine the time course and duration of response, including stressor type, and the status of a particular system at the time of stressor presentation. We briefly review data indicating that CRH mediates physiological and behavioral responses to stressors, and present new data supporting the hypothesis that CRH may also be involved in the physiological regulation of waking.

Animals↗
PubMed1995

Influence of host defense activation on sleep in humans.

Despite considerable progress in our understanding of the phenomenology of sleep and wakefulness, their regulation and peculiar functions are poorly understood. Recent animal research has revealed considerable evidence for interactions between host defense and sleep. Therefore, it has been hypothesized that host response mediators, mainly cytokines like interleukin-1 (IL-1), are involved in physiological sleep regulation. Furthermore, it has been suggested that sleep, and non rapid eye movement (NREM) sleep in particular, has an immuno-supportive function. In humans, sleep-host defense interactions are just starting to be understood. There is quite good evidence that some viral diseases cause excessive sleepiness. Other infectious diseases induce, however, serious disturbances of the distribution of sleep and wakefulness rather than excessive sleep. In addition, some disorders with excessive sleep, daytime fatigue or disturbed night sleep as prominent symptoms are thought to involve, at least in part, immuno-pathophysiological mechanisms. Experimental settings have only recently been used to elucidate host defense-sleep interactions in humans. The effects of endotoxin, a cell-wall lipopolysaccharide of gram-negative bacteria, on sleep have been tested in different settings in healthy volunteers. Endotoxin transiently suppresses rapid eye movement (REM) sleep independently of the time of the day of administration. Only low doses, given in the evening, promote NREM sleep. Electorencephalogram (EEG) power in higher frequency bands is enhanced during NREM sleep, whereas delta activity is not affected. In rats and rabbits, on the other hand, the effects of endotoxin and of the mediators of its activity on REM sleep are variable. Enhanced NREM sleep is a common finding and most pronounced during the active part of the nycthemeron and, in general, EEG delta activity is augmented. In view of these species differences, hypotheses regarding the underlying mechanisms and the biological significance of host defense-sleep interactions, primarily derived from the results of animal studies, may not entirely fit human physiology. They should therefore be re-evaluated and probably modified, through the use of additional experimental approaches in humans.

Animals↗
PubMed1995

Cytokines in sleep regulation.

The central thesis of this essay is that the cytokine network in brain is a key element in the humoral regulation of sleep responses to infection and in the physiological regulation of sleep. We hypothesize that many cytokines, their cellular receptors, soluble receptors, and endogenous antagonists are involved in physiological sleep regulation. The expressions of some cytokines are greatly amplified by microbial challenge. This excess cytokine production during infection induces sleep responses. The excessive sleep and wakefulness that occur at different times during the course of the infectious process results from dynamic changes in various cytokines that occur during the host's response to infectious challenge. Removal of any one somnogenic cytokine inhibits normal sleep, alters the cytokine network by changing the cytokine mix, but does not completely disrupt sleep due to the redundant nature of the cytokine network. The cytokine network operates in a paracrine/autocrine fashion and is responsive to neuronal use. Finally, cytokines elicit their somnogenic actions via endocrine and neurotransmitter systems as well as having direct effects neurons and glia. Evidence in support of these postulates is reviewed in this essay.

Acute-Phase Reaction↗
PubMed1995

Morphine stimulates phagocytosis of Mycobacterium tuberculosis by human microglial cells: involvement of a G protein-coupled opiate receptor.

Opiate-induced immunosuppression has been implicated in the pathogenesis of infections caused by a variety of microorganisms, including human immunodeficiency virus (HIV). Although effects of opiates on lymphocyte function have been studied more extensively, morphine also has been shown to inhibit several functional activities of mononuclear phagocytes (e.g. chemotaxis, respiratory burst activity and phagocytosis). Opiate addiction has been identified as a risk factor for clinical tuberculosis prior to the HIV epidemic, and macrophages are a key cell in the pathogenesis of Mycobacterium tuberculosis. Thus, the hypothesis was tested in the present study that morphine would suppress phagocytosis of M. tuberculosis by human microglial cells, the resident macrophages of the brain. Contrary to this hypothesis, treatment of human fetal microglial cell cultures with morphine (10(-8) M) was found to stimulate phagocytosis of nonopsonized M. tuberculosis H37Rv. The stimulatory effect of morphine was blocked by naloxone and the mu opiate receptor selective antagonist beta-funaltrexamine. Also, morphine-induced increase in phagocytic activity was markedly inhibited by pertussis toxin and was unaffected by cholera toxin, suggesting the mechanism of morphine's stimulatory effect on microglial cell phagocytosis involves a Gi protein-coupled mu opiate receptor. The results of this in vitro study support the concept that exogenous and endogenous opioids play an immunomodulatory role within the central nervous system through their interaction with G protein-coupled receptors on microglial cells.

Adjuvants, Immunologic↗
PubMed1995

Mechanisms for nitric oxide-induced cell death: involvement of apoptosis.

Recent observations suggest that apoptosis, the natural, active cell death process is also triggered in several pathological conditions including ischemic brain insult, and neuro-degenerative and autoimmune diseases. We have investigated the mechanisms involved in the development of apoptosis in neuronal and pancreatic cells and in macrophages, which were exposed to either chemical donors of nitric oxide or to inducers of the nitric oxide synthase. In this overview, we summarize current evidence for the involvement of apoptosis in the cytotoxicity of nitric oxide and discuss possible mechanisms that may lead to cell death.

AIDS Dementia Complex↗
PubMed1996

The neuroimmunology of multiple sclerosis.

The aim of this clinical review is to highlight recent advances in immunology, as well as new information from selected other areas, which have led to a better appreciation of the neuroimmunologic mechanisms involved in Multiple sclerosis (MS). New data on immunopathology, the cytokine network, and the role of oligodendrocytes, lymphocytes, and endothelial cells in this disease, have produced novel therapeutic approaches. New information on clinical course and neuroimaging disease features, as well as the role of genetic factors and infectious agents, have also improved our understanding of the immune basis for MS.

Adult↗
PubMed1996

Psychoneuroimmunology of autoimmune disorders.

The interactions between the immune system and psychological states are both intricate and intriguing. Research at a molecular level has thrown considerable light on the previously ill-defined area of psychoneuroimmunology. In this report, we explore the psychoneuroimmunology of autoimmune disorders, particularly rheumatoid arthritis and lupus erythematosus. Animal models of these diseases have provided a particularly useful window on complex psychoneuroimmunological interactions. Observations about the effect of stress on the onset and course of autoimmune disorders has added to our understanding of psychoneuroimmunological interactions. These interactions are bi-directional, as reflected in the autoimmune-mediated neuropsychiatric manifestations of systemic lupus. Exploring the role of various neurotransmitters and neuromodulators in the stress response may have important therapeutic implications for autoimmune disorders.

Animals↗
PubMed1996

Psychoneuroimmunology and cancer: historical perspectives and current research.

The belief that cancer might be related to temperament or distress has been emphasized throughout the history of medicine. The field of psychoneuroimmunology has its origins in psychosomatic medicine, and has evolved to the investigations of complex interactions between the psyche and the nervous, immune, and endocrine systems. Such interactions may have implications in both cancer risk and survival.

Bereavement↗
PubMed1995

Visible light induced changes in the immune response through an eye-brain mechanism (photoneuroimmunology).

The immune system is susceptible to a variety of stresses. Recent work in neuroimmunology has begun to define how mood alteration, stress, the seasons, and daily rhythms can have a profound effect on immune response through hormonal modifications. Central to these factors may be light through an eye-brain hormonal modulation. In adult primates, only visible light (400-700 nm) is received by the retina. This photic energy is then transduced and delivered to the visual cortex and by an alternative pathway to the suprachiasmatic nucleus (SCN). The SCN is a part of the hypothalamic region in the brain believed to direct circadian rhythm. Visible light exposure also modulates the pituitary and pineal gland which leads to neuroendocrine changes. Melatonin, norepinephrine and acetylcholine decrease with light activation, while cortisol, serotonin, gaba and dopamine levels increase. The synthesis of vasoactive intestinal polypeptide (VIP), gastrin releasing peptide (GRP) and neuropeptide Y (NPY) in rat SCN has been shown to be modified by light. These induced neuroendocrine changes can lead to alterations in mood and circadian rhythm. All of these neuroendocrine changes can lead to immune modulation. An alternative pathway for immune modulation by light is through the skin. Visible light (400-700 nm) can penetrate epidermal and dermal layers of the skin and may directly interact with circulating lymphocytes to modulate immune function. However, even in the presence of phototoxic agents such as eosin and rose bengal, visible light did not produce suppression of contact hypersensitivity with suppresser cells. In contrast to visible light, in vivo exposure to UV-B (280-320 nm) and UV-A (320-400 nm) radiation can only alter normal human immune function by a skin mediated response. Each UV subgroup (B, A) induces an immunosuppressive response but by differing mechanisms involving the regulation of differing interleukins and growth factors. Some effects observed in humans are: inhibition of allergic contact dermatitis; inhibition of delayed hypersensitivity to an injected antigen; prolongation of skin-graft survival and induction of a tumor-susceptible state. The following article will review much of the progress in this field and explore possible areas of future research.

Animals↗
PubMed2005

Acupuncture and kidney disease.

Acupuncture as a complex therapeutic system has been used to treat a variety of diseases and pathological conditions. Although the exact mechanism(s) of acupuncture remains unknown, some evidence suggests a mechanism initially involving signal transduction through connective tissue, with secondary involvement of other systems including the nervous system. Acupuncture has become increasingly popular in the Western countries as a therapy for pain and several chronic disorders difficult to manage with conventional treatments. Acupuncture and acupuncture-like somatic nerve stimulation have been used in different kidney diseases and several complications related to them. The effect of acupuncture techniques in some kidney diseases is reviewed on the basis of clinical reports as well as mechanisms that may possibly explain the beneficial effects mediated by acupressure/acupuncture. The potential effect of acupressure techniques in renal inflammation and whether these effects could be mediated through the newly identified cholinergic anti-inflammatory pathway are discussed.

Acupuncture Therapy↗
PubMed2006

Anxiety-induced plasma norepinephrine augmentation increases reactive oxygen species formation by monocytes in essential hypertension.

BACKGROUND: An association between anxiety and depression and increased blood pressure (BP) and cardiovascular disease risk has not been firmly established. We examined the hypothesis that anxiety and depression lead to increased plasma catecholamines and to production of reactive oxygen species (ROS) by mononuclear cells (MNC) in hypertensive individuals. We also studied the role of BP in this effect. METHODS: In Protocol 1, a cross-sectional study was performed in 146 hypertensive patients to evaluate whether anxiety and depression affect BP and ROS formation by MNC through increasing plasma catecholamines. In Protocol 2, a 6-month randomized controlled trial using a subtherapeutic dose of the alpha(1)-adrenergic receptor antagonist doxazosin (1 mg/day) versus placebo in 86 patients with essential hypertension was performed to determine whether the increase in ROS formation by MNC was independent of BP. RESULTS: In Protocol 1, a significant relationship was observed between the following: trait anxiety and plasma norepinephrine (r = 0.32, P < .01); plasma norepinephrine and ROS formation by MNC (r = 0.36, P < .01); and plasma norepinephrine and systolic, diastolic, and mean BP (r = 0.17, P = .04; r = 0.26, P = .02; r = 0.23, P < .01, respectively). In Protocol 2, subtherapeutic doxazosin treatment (1 mg/day) had no significant effect on BP. However doxazosin significantly decreased ROS formation by MNC compared with placebo (P < .01). CONCLUSION: Trait anxiety may increase plasma norepinephrine and increase ROS formation by MNC independent of BP in hypertensive patients.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed2005

Novel pathway for LPS-induced afferent vagus nerve activation: possible role of nodose ganglion.

The afferent vagus nerve has been suggested to be an important component for transmitting peripheral immune signals to the brain. However, there is inconsistent evidence showing that subdiaphragmatic vagotomy did not inhibit the brain mediated behavioral and neural effects induced by the peripheral application of lipopolysaccharide (LPS). LPS triggers innate immune cells through Toll-like receptor 4 (TLR4). In the present study, we found that TLR4 mRNA and protein was expressed in the rat nodose ganglion. Thus, it is suggested that LPS could activate afferent vagus nerve at the level of nodose ganglion, which exists centrally from the subdiaphragmatic level of vagus nerve. The results could provide evidence for the novel pathway of LPS-induced afferent vagus nerve activation.

Animals↗
PubMed2004

Is autism an autoimmune disease?

Autism spectrum disorder (ASD) is a spectrum of behavioral anomalies characterized by impaired social interaction and communication, often accompanied by repetitive and stereotyped behavior. The condition manifests within the first 3 years of life and persists into adulthood. There are numerous hypotheses regarding the etiology and pathology of ASD, including a suggested role for immune dysfunction. However, to date, the evidence for involvement of the immune system in autism has been inconclusive. While immune system abnormalities have been reported in children with autistic disorder, there is little consensus regarding the nature of these differences which include both enhanced autoimmunity and reduced immune function. In this review, we discuss current findings with respect to immune function and the spectrum of autoimmune phenomena described in children with ASD.

Autistic Disorder↗
PubMed2003

Sleep-deprived mice show altered cytokine production manifest by perturbations in serum IL-1ra, TNFa, and IL-6 levels.

Serum cytokine and chemokine levels were examined in mice following 36 h of sleep deprivation, or after exposure to a known physical stressor (rotational stress). Significant changes in inflammatory cytokines/chemokines (IL-1beta, TNFalpha, IL-1ra, IL-6, and MIP-1beta, MCP-1) were observed following each manipulation, but qualitative and quantitative differences were seen. Interestingly, only physical stress was associated with measured increases in serum corticosterone levels, and with independent evidence (using in vitro immune allostimulation) for a generalized immunosuppression secondary to the experimental manipulation. Our data suggest that altered cytokine production following sleep perturbation occurs by a different mechanism from that (HPA axis) commonly attributed to stress per se.

Acebutolol↗
PubMed2004

Stress-induced enhancement of NF-kappaB DNA-binding in the peripheral blood leukocyte pool: effects of lymphocyte redistribution.

To identify signaling pathways by which the sympathetic nervous system (SNS) might alter gene expression in the immune system, we assayed activation of the inflammatory transcription factor NF-kappaB in peripheral blood mononuclear cells (PBMC) from 13 healthy young adults at rest and following 5 min of intense exercise. SNS activation was verified by changes in cardiovascular parameters and mobilization of NK cells into circulating blood. Electrophoretic mobility shift assays (EMSA) of nuclear protein extracts confirmed previous findings that SNS activation increased NF-kappaB DNA-binding activity in bulk PBMC. However, analyses of isolated leukocyte subsets failed to indicate any increase on a per-cell basis in NK cells (the major carriers of NF-kappaB activity in circulating PBMC), in the residual CD56- leukocyte pool, or in CD14+ monocytes. Regression analyses indicated a strong correlation between increasing NK cell prevalence and changes in NF-kappaB DNA-binding activity in bulk PBMC, and suggested that no change in EMSA activity would be observed in the absence of NK cell mobilization. Such results imply that SNS-induced mobilization of NK cells can rapidly (< 10 min) alter NF-kappaB DNA-binding activity in the circulating PBMC pool without generating any true change in NF-kappaB activity on a per-cell basis. Implications for future efforts to analyze stress effects on leukocyte gene expression are considered.

Adaptation, Physiological↗
PubMed2004

Brain response to cecal infection with Campylobacter jejuni: analysis with Fos immunohistochemistry.

Infections with bacterial pathogens can induce increased anxiety-like behaviors in rodents without otherwise noticeable behavioral or physiological symptoms of sickness, as shown with the food-borne pathogen Campylobacter jejuni. This observation implicates the ability of the brain to sense, and respond to, such an infection. We tested our hypothesis that intestinal infection with the gram-negative bacterium C. jejuni leads to activation of certain brain regions that process gastro-intestinal sensory information. The induction of c-Fos protein as a marker for neuronal activation was assessed in the brains of mice inoculated orally with live C. jejuni, as compared to saline-treated controls. Upon colonization of the intestines, C. jejuni activated visceral sensory nuclei in the brainstem (the nucleus of the solitary tract and the lateral parabrachial nucleus) both one and two days after the oral challenge. In addition, increased c-Fos expression occurred in the hypothalamic paraventricular nucleus on the second day. This neural response occurred in the absence of measurable systemic immune activation, as serum levels of tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6 were undetectable and/or unchanged. These findings support the notion that information about infection with C. jejuni in the gut is indeed relayed to the visceral sensory structures in the brain. The brain responses observed could contribute to changes in behavior observed after infection.

Analysis of Variance↗