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PubMed2004

Alcoholism and neuro-immune-endocrine interactions: physiochemical aspects.

The role of alcohol consumption and alcoholism as an addiction in regulating the chemistry of the brain and its physiology has gained a backlog of interest over the past few decades. Besides the notion that alcohol acts as a brain depressant, the molecular mechanisms and neuronal interactions are not well understood. Emerging evidence implicates alcohol as a neurochemical messenger that influences a cross talk amongst the nervous, immune, and endocrine systems. Specifically, alcohol acts as a crucial regulator of the hypothalamic-pituitary-adrenal (HPA) axis, thereby modulating the release of hormones, particularly adrenocorticotropic hormone (ACTH) and corticosterone (CORT). It is the aim of this review, therefore, to investigate current concepts on how alcohol, particularly ethanol, and alcoholism affect neuro-immune-endocrine neurochemical interactions via the regulation of the HPA axis, taking into consideration bio-behavioral and physiochemical aspects.

Adrenocorticotropic Hormone↗
PubMed2006

Intestinal neuro-epithelial interactions modulate neuronal chemokines production.

Human enteric neurons have recently been shown to produce chemokines during intestinal inflammation. However, whether (1) neuro-epithelial interactions modulate neuronal chemokines production and (2) neurons can induce the chemotaxis of immune cells remain unknown. Neuro-epithelial interactions were studied using a coculture model composed of human neurons (NT2-N) and intestinal epithelial cells (Caco-2). IL-8 or MIP-1beta expression was analyzed by quantitative-PCR, ELISA or immunohistochemistry. Neuronally induced chemotaxis was studied using a coculture model composed of NT2-N and human peripheral blood mononuclear cells (PBMC). Following Caco-2 inflammation with IFNgamma/TNFalpha, neuronal IL-8 and MIP-1beta mRNA expression was significantly increased compared to control. This increase was significantly reduced by IL-1 receptor antagonist. IL-1beta-pretreated NT2-N induced the chemotaxis of PBMC, which was significantly reduced by anti-IL-8, but not by anti-MIP-1beta neutralizing antibody. Our results demonstrate that, under inflammatory conditions, neuro-epithelial interactions can modulate neuronal chemokines production through IL-1beta-dependent pathways. Furthermore, neuronal IL-1beta-induced chemotactic properties could favor the development of immune cells infiltrates within the enteric nervous system, as is observed during intestinal inflammation.

Cell Communication↗
PubMed2004

Different approaches to understanding autoimmune rheumatic diseases: the neuroimmunoendocrine system.

Rheumatic autoimmune diseases are characterized by dysregulation of the immune response that leads to inflammation, pain, disease and stiffness and have been shown to have differences in disease pattern, depending on the gender and age of an individual. The majority of these conditions predominantly affect females of all species and also show increased severity of disease in female animal models. In addition to the gender differences in disease development, persons are often more susceptible at specific stages of life. This review will discuss some of the data indicating age and gender differences in development of these diseases and will review hormonal and other factors that may contribute to disease expression and severity.

Animals↗
PubMed2004

Neuroimmune and cortisol changes in selective serotonin reuptake inhibitor and placebo treatment of chronic posttraumatic stress disorder.

BACKGROUND: To explore relations between neuroimmune and neuroendocrine systems relative to posttraumatic stress disorder (PTSD) treatment, cortisol and cytokine changes in response to selective serotonin reuptake inhibitor (SSRI) and placebo treatment of chronic PTSD were assessed prospectively. METHODS: Baseline measures of PTSD, depression, salivary 8 am and 4 pm cortisol, and serum interleukin-1beta (IL-1beta; pro-inflammatory) and soluble interleukin-2 receptors (IL-2R; cell-mediated immunity) were obtained for 58 PTSD and 21 control subjects. The PTSD subjects participated in a 10-week, double-blind treatment with citalopram (n = 19), sertraline (n = 18), or placebo (n = 7). RESULTS: At baseline, PTSD subjects had significantly greater PTSD, depression, and IL-1beta and lower IL-2R levels than control subjects, with no group differences found for am or pm cortisol levels. Both SSRI groups' IL-1beta correlated negatively with IL-2R; neither cytokine correlated with cortisol levels. Treatment significantly lowered PTSD, depression, and IL-1beta levels and increased IL-2R for all groups to control subject levels. After treatment, both SSRI groups' IL-1beta correlated with an end cortisol measure (one negatively, one positively). CONCLUSIONS: Our results support a complex relationship between neuroimmune and neuroendocrine systems with PTSD treatment. Implications of normalization of cytokine levels with effective SSRI treatment and placebo are discussed.

Adult↗
PubMed2005

Immune activation during pregnancy in mice leads to dopaminergic hyperfunction and cognitive impairment in the offspring: a neurodevelopmental animal model of schizophrenia.

BACKGROUND: Maternal viral infection is associated with increased risk for schizophrenia. It is hypothesized that the maternal immune response to viruses may influence fetal brain development and lead to schizophrenia. METHODS: To mimic a viral infection, the synthetic double strand RNA polyriboinosinic-polyribocytidilic acid (poly I:C) was administered into pregnant mice. Behavioral evaluations (thigmotaxis, methamphetamine [MAP]-induced hyperactivity, novel-object recognition test [NORT]), sensorimotor gating (prepulse inhibition [PPI]), and biochemical evaluation of the dopaminergic function of the offspring of phosphate-buffered saline (PBS)-treated dams (PBS-mice) and that of poly I:C-treated dams (poly I:C-mice) were examined. RESULTS: In juveniles, no difference was found between the poly I:C-mice and PBS-mice. However, in adults, the poly I:C-mice exhibited attenuated thigmotaxis, greater response in MAP-induced (2 mg/kg) hyperlocomotion, deficits in PPI, and cognitive impairment in NORT compared with the PBS-mice. Cognitive impairment in the adult poly I:C-mice could be improved by subchronic administration of clozapine (5.0 mg/kg) but not haloperidol (.1 mg/kg). Increased dopamine (DA) turnover and decreased receptor binding of D2-like receptors, but not D1-like receptors, in the striatum were found in adult poly I:C-mice. CONCLUSIONS: Prenatal poly I:C administration causes maturation-dependent increased subcortical DA function and cognitive impairment in the offspring, indicating a neurodevelopmental animal model of schizophrenia.

Animals↗
PubMed2004

Paraventricular nucleus neurons producing neurotensin after lipopolysaccharide treatment project to the median eminence.

Inflammation consists in secretion of cytokines that stimulate the hypothalamo-pituitary-adrenal (HPA) axis to release the anti-inflammatory corticosterone. Upstream in this axis are corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus (PVN) whose multipeptidergic phenotype changes: both corticotropin-releasing hormone mRNAs and neurotensin mRNAs are up-regulated. Combining in situ hybridization with a retrograde neuronal marker, we demonstrated that neurotensin-containing neurons in the paraventricular nucleus project to the median eminence.

Acute-Phase Reaction↗
PubMed2005

Changes in hippocampal IL-15, related cytokines, and neurogenesis in IL-2 deficient mice.

Previous studies have demonstrated that interleukin-2 knockout (KO) mice exhibit alterations in hippocampal cytoarchitecture. Several lines of evidence suggest that these variations may result from immune dysregulation and/or autoimmunity. Thus, this study sought to compare adult IL-2 KO mice and wild-type littermates (8-12 weeks of age), the age where differences in hippocampal cytoarchitecture have previously been observed, for differences in measures of neuroimmunological status in the hippocampus. Furthermore, because IL-15 shares the same receptor subunits for signal transduction as IL-2 (IL-2/15Rbeta and gammac) that are enriched in the hippocampus and may induce inflammatory processes in IL-2 KO mice, we sought to test the hypothesis that IL-15 is elevated in the hippocampus of IL-2 KO mice. Compared to wild-type mice, IL-2 KO mice exhibited increased hippocampal protein concentrations of IL-15 as well as IL-12, IP-10, and MCP-1. These cytokine changes, however, did not correlate with levels in the peripheral circulation, and there were no T cells or an increase in MHCII-positive microglia in the hippocampus of IL-2 KO mice. Since elevated levels of certain inflammatory cytokines may impair hippocampal neurogenesis, we also tested the hypothesis that changes in neuroimmunological status would be associated with reductions in neurogenesis of neurons in the dentate gyrus of IL-2 KO mice. Contrary to this hypothesis, compared to wild-type mice, male IL-2 KO mice exhibited increased neurogenesis in both the infrapyramidal and suprapyramidal limbs of the granule cell layer of the dentate gyrus, differences that were not observed between females. These findings indicate that IL-2 gene deletion alters the neuroimmunological status of the mouse hippocampus through a dysregulation of cytokines produced by CNS cells, and in males, these changes are associated with increased hippocampal neurogenesis.

Animals↗
PubMed2006

Organization of immune-responsive medullary projections to the bed nucleus of the stria terminalis, central amygdala, and paraventricular nucleus of the hypothalamus: evidence for parallel viscerosensory pathways in the rat brain.

Immune-responsive neurons in the brainstem, primarily in the nucleus of the solitary tract (NTS) and ventrolateral medulla (VLM), contribute to a significant drive on forebrain nuclei responsible for brain-mediated host defense responses. The current study investigated the relative contribution of brainstem-derived ascending pathways to forebrain immune-responsive nuclei in the rat by means of retrograde tract tracing and c-Fos immunohistochemistry. Fluorogold was iontophoresed into the bed nucleus of stria terminalis (BST), central nucleus of the amygdala (CEA), paraventricular nucleus of the hypothalamus (PVN), and the pontine lateral parabrachial nucleus (PBL; an important component of ascending viscerosensensory pathways) followed 2 weeks later by intraperitoneal injection of lipopolysaccharide (LPS, 0.1 mg/kg) or saline. The NTS and VLM provide immune-responsive input to all four regions, via direct, predominantly catecholaminergic, projections to the PVN, the lateral BST, and the CEA, and mostly non-catecholaminergic projections to the PBL. The PBL provides a major LPS-activated input to the BST and CEA. The pattern of LPS-activated catecholaminergic projections from the VLM and NTS to the forebrain is characterized by a strong predominance of VLM input to the PVN, whereas the NTS provides a greater contribution to the BST. These findings indicate that direct and indirect pathways originate in the caudal brainstem that propagate immune-related information from the periphery with multiple levels of processing en route to the forebrain nuclei, which may allow for integration of brain responses to infection.

Amygdala↗
PubMed2003

Chronic psychosocial stress down-regulates central cytokines mRNA.

Brain cytokines have been implicated in brain plasticity and mood alterations. We present here the first evidence of a chronic stress-induced modulation of central cytokines, in absence of experimentally induced inflammatory processes. Several brain areas were extracted from stressed and control mice and cytokines mRNA analyzed with semi-quantitative RT-PCR. Mice subjected to chronic psychosocial stress showed decreased interleukin (IL)-1beta mRNA levels in the hippocampus, decreased IL-1Receptor antagonist in the striatum and pituitary, decreased tumor necrosis factor (TNF)-alpha in the striatum and hippocampus, and decreased glucocorticoid receptor (GR) in the striatum and hippocampus compared to group housed sibling mice. An independent group of mice subjected to chronic psychosocial stress also showed increased plasma corticosterone. These findings may open new perspectives for understanding the pathophysiological basis of chronic stress-induced disorders.

Animals↗
PubMed2005

The role of mast cells in migraine pathophysiology.

Mast cells are critical players in allergic reactions, but they have also been shown to be important in immunity and recently also in inflammatory diseases, especially asthma. Migraines are episodic, typically unilateral, throbbing headaches that occur more frequently in patients with allergy and asthma implying involvement of meningeal and/or brain mast cells. These mast cells are located perivascularly, in close association with neurons especially in the dura, where they can be activated following trigeminal nerve, as well as cervical or sphenopalatine ganglion stimulation. Neuropeptides such as calcitonin gene-related peptide (CGRP), hemokinin A, neurotensin (NT), pituitary adenylate cyclase activating peptide (PACAP), and substance P (SP) activate mast cells leading to secretion of vasoactive, pro-inflammatory, and neurosensitizing mediators, thereby contributing to migraine pathogenesis. Brain mast cells can also secrete pro-inflammatory and vasodilatory molecules such as interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF), selectively in response to corticotropin-releasing hormone (CRH), a mediator of stress which is known to precipitate or exacerbate migraines. A better understanding of brain mast cell activation in migraines would be useful and could lead to several points of prophylactic intervention.

Animals↗
PubMed2004

Neuroimmunology of the paraneoplastic neurological degenerations.

The paraneoplastic neurological degenerations (PNDs) are remarkable examples of naturally occurring tumor immunity in humans. In PND patients, common tumors such as breast, ovarian and lung tumors express proteins normally made exclusively in the brain, eliciting an immune response that successfully suppresses growth of the tumor. This successful anti-tumor response would be expected to go clinically unnoticed by the patient, but the immune cells mediating the response somehow cross into the brain, resulting in an autoimmune attack on neurons and neurological symptoms. Pieces of the mystery of this tumor immune response and neuronal autoimmunity have been assembled, but much more needs to be learned.

Animals↗
PubMed2005

Stress and psychoneuroimmunologic factors in dermatology.

There is clinical and experimental evidence that the brain can start, influence, and stop biologic skin events. Studies suggest that the skin, as a relevant part of the "diffuse brain," can modify the quality of perceptions and feelings. The immune and the endocrine systems seem to represent the protagonists of the modulation of those events and, in this context, psychosocial stressors and interventions can lead to global health changes of great interest for dermatologists.

Dermatology↗
PubMed2005

Psychoneuroimmunodermatology of atopic dermatitis: from empiric data to the evolutionary hypothesis.

Atopic dermatitis is a pruritic skin disease affecting predominantly young people. There is evidence that psychologic stress constitutes an increased risk for atopy and influences the disease's clinical course. This risk is believed mediated by the effects of stress on neuroimmunoregulation, which in turn modulates the hypersensitivity response and involves immunoglobulin E-mediated inflammation, helper T-cell 2 predominance, and eosinophilia. This article examines theoretic perspectives and other behavioral dimensions, such as maternal caring behavior, infant response to stress, temperament, and the so-called "hygiene hypothesis." The Darwinian framework and the mental scenario are examined. These processes may be akin to the generation of antibodies by the immune system.

Dermatitis, Atopic↗
PubMed2004

Cytokine-induced sickness behaviour: a neuroimmune response to activation of innate immunity.

Sickness refers to a coordinated set of subjective, behavioural and physiological changes that develop in sick individuals during the course of an infection. These changes are due to the effects of interleukin-1 (IL-1) and other proinflammatory cytokines on brain cellular targets. Sickness behaviour is mediated by proinflammatory cytokines that are temporarily expressed in the brain during infection. These centrally produced cytokines are the same as those expressed by innate immune cells and they act on brain receptors that are identical to those characterized on immune cells. Primary afferent nerves represent the main communication pathway between peripheral and central cytokines. Proinflammatory cytokines modulate learning and memory processes. The expression and action of proinflammatory cytokines in the brain in response to peripheral cytokines are regulated by various molecular intermediates including anti-inflammatory cytokines such as interleukin-10 (IL-10) and the IL-1 receptor antagonist (IL-1ra), growth factors such as insulin-like growth factor-1 (IGF-1), hormones such as glucocorticoids and neuropeptides such as vasopressin and alpha-melanotropin.

Animals↗
PubMed2004

Secretion of IgA by rat parotid and submandibular cells in response to autonomimetic stimulation in vitro.

The major antibody in saliva is IgA, which is actively transported by pIgR expressed by parenchymal cells within the salivary glands. The rate of IgA secretion into saliva is regulated by the autonomic nerves supplying the glands in vivo. This study examined the mechanism of increased IgA secretion into saliva with autonomimetic stimulation. In vitro stimulation of IgA secretion from cells prepared by digestion of rat salivary glands found submandibular cell preparations responded to alpha- and beta-adrenergic stimuli whereas the parotid cells responded only to beta-adrenergic stimulation, although cells from both glands responded similarly to cholinergic stimulation. The additional responsiveness of submandibular cells to alpha-adrenergic stimulation probably reflects the presence of granular duct cells (absent in parotid glands) which are known to secrete protein in response to high frequency sympathetic stimulation. The increased secretion of IgA was not dependant upon increased plasma cell activation since isolated salivary gland plasma cells did not respond to agonists. Further evidence for the regulating role of parenchymal cells in IgA secretion into saliva was revealed by analysis of polymeric immunoglobulin receptor (pIgR) levels expressed on cells. Following in vivo nerve stimulation, there was an increased amount of pIgR expressed on the membrane surface. This was functionally demonstrated in vitro by increased uptake of human IgA by acutely prepared rat salivary cells following stimulation by adrenaline, indicating increased mobilisation of pIgR with stimulation. This study confirms that salivary cells increase the delivery of IgA into saliva by a pIgR-mediated mechanism in response to autonomic stimulation.

Adrenergic beta-Agonists↗
PubMed2003

Is innervation an early target in autoimmune diabetes?

In the non-obese diabetic (NOD) mouse, a spontaneous model of type 1 diabetes (T1D), recent evidence suggests that Schwann cells (Scs) and neurons surrounding insulin-producing beta cells of the islets of Langerhans are destroyed before beta cells. During normal perinatal development, macrophages (MPhi) are involved in phagocytosis of apoptotic neurons. Pertinently, MPhi are already present at birth in NOD pancreata. Their possible abnormal control of nerve phagocytosis, together with transient beta-cell hyperactivity and lymphocyte anomalies, might conjointly participate in T1D pathogenesis.

Animals↗