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Results for “Neuroimmunomodulation”

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At least 73 records · Page 4Linked to original sources
PubMed2000

Control of salivary secretion by nitric oxide and its role in neuroimmunomodulation.

In many in vivo systems exposure to endotoxins (LPS) leads to the co-induction of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), which is important to the regulation of the function of different systems during infection. In submandibular glands (SMG) neural (n)NOS is localized in neural terminals and in striated, granular convoluted and excretory ducts, endothelial (e)NOS in vascular endothelium and ducts, and iNOS in macrophages and in tubules and ducts. In normal adult male rats, injection of an inhibitor of NOS decreased the stimulated salivary secretion and a donor of NO potentiated it, indicating that NO exerts a stimulatory role. A single high dose of LPS (5 mg/kg, i.p.) induced an increase in NOS activity measured by the 14C-citrulline method, increased PGE content almost 100% as measured by RIA, and blocked stimulated salivary secretion. The administration of a specific iNOS inhibitor, aminoguanidine (AG), with LPS not only decreased NOS activity but significantly decreased PGE content, indicating that NO triggered the activation of COX-2. LPS increased conversion of labeled arachidonate to prostaglandins (PGs) showing that COX was induced. Since a PGE1 analogue blocked stimulated salivation, the LPS-induced inhibition of salivation is probably due to release of PGs. Therefore, the use of inhibitors of iNOS and COX-2 could be very useful to increase salivation during infection since saliva has antimicrobial actions.

Animals↗
PubMed2000

Neuropeptide control of bone marrow neutrophil production. A key axis for neuroimmunomodulation.

Nerve fibers project into the bone marrow and terminate in association with stromal cells. Nerve terminals are also associated with antigen-processing and -presenting cells throughout the body and have been shown to be important in leukocyte trafficking and wound healing as well as hemopoiesis. Here we show that neuropeptide input to the bone marrow is vital to normal granulopoiesis and that deletion of the neuropeptides, substance P, and calcitonin gene-related peptide (CGRP), with the neurotoxin, capsaicin, abrogates normal blood cell production. Norepinephrine, neurokinins a and 2, and vasoactive intestinal peptide all have inhibitory effects on in vitro CFU-GM colony formation. Substance P, neurokinin 1, nerve growth factor, and CGRP have stimulatory effects on CFU-GM. Furthermore, in vitro experiments show that, apart from CGRP, all the neuroactive substances we tested operate through effects on accessory cells, stimulating the release of regulatory molecules that have a direct effect on purified CFU-GM.

Animals↗
PubMed2000

Complex coping patterns and their role in adaptation and neuroimmunomodulation. Theory, methodology, and research.

This paper describes the evolution of a model of adaptative coping, as well as an example of the converse, a maladaptive coping pattern, type C. It was hypothesized that the more closely a coping process resembles the inverted U-shaped function that characterizes homeostasis for most biological systems, the more likely it is to be adaptive, and to be associated with more positive health outcomes. Maladaptive learned coping patterns, such as type C coping, represent deviations from homeostasis in that they fail to recognize, respond appropriately to, and/or resolve stressors, thus keeping the physiological stress response chronically engaged, with subsequent long-term damage to implicated biological systems. This interpretation of how maladaptive coping patterns such as type C can influence health outcomes is consistent with findings from the author's 20-year program of research on the type C pattern, its assessment, and its association with poorer health indicators and outcomes in cancer (malignant melanoma) and HIV/AIDS.

Adaptation, Psychological↗
PubMedDate not supplied

Lateralization and catecholaminergic neuroimmunomodulation: prazosin, an alpha1/alpha2-adrenergic receptor antagonist, suppresses interleukin-1 and increases interleukin-10 production induced by lipopolysaccharides.

OBJECTIVE: The brain has previously been shown to asymmetrically modulate neurochemical, neuroendocrine and immune responses to lipopolysaccharides (LPS). As these responses are reversed by a chemical sympathectomy, it can be hypothesized that the asymmetry in the functioning of the sympathetic nervous system may be one of the mechanisms by which the brain hemispheres asymmetrically modulate immune reactivity. METHODS: The effects of prazosin, an alpha1/alpha2-adrenergic receptor antagonist, on the production of interleukin (IL)-1beta and IL-10 induced by LPS was studied in mice selected for their paw preference. RESULTS: Two hours after intraperitoneal injection of 5 microg of LPS, plasma levels of IL-1beta were higher in right-pawed mice as compared to left-pawed or ambidextrous animals. No lateralization effect was observed for LPS-induced plasma IL-10 levels. Prazosin, 10 mg/kg, injected intraperitoneally half an hour before LPS, reduced plasma levels of IL-1beta and abolished the effect of lateralization. By contrast, prazosin drastically increased plasma levels of IL-10 in response to LPS and the production of corticosterone in untreated controls. CONCLUSIONS: These results suggest that the catecholaminergic modulation of immune reactivity depends on lateralization. This work further demonstrates that prazosin is endowed with anti-inflammatory properties that may be considered side effects of this drug, which is widely prescribed in the treatment of hypertension.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Neuroimmunomodulation and immune privilege: the role of neuropeptides in ocular immunosuppression.

Regional immunoregulatory mechanisms insure that the most effective immune defense mounted is in proportion with preserving unique tissue functionalities. Immune-privileged tissues, such as the eye, are tissue sites of extreme regional immunoregulation. They have evolutionarily adapted several mechanisms to prevent the induction of inflammation within their tissue microenvironment. With over half a century of experimental examinations of ocular immune privilege, only recently have we come to understand that neuropeptides constitutively present in ocular tissues are part of the mechanisms of immune privilege.

Animals↗
PubMedDate not supplied

Evidence for hypothalamic paraventricular nucleus as an integrative center of neuroimmunomodulation.

It has been well documented that the medial parvocellular subnucleus of the hypothalamic paraventricular nucleus (PVN) participates in immune regulation by releasing corticotrophin-releasing hormone (CRH), which triggers the hypothalamus-pituitary-adrenal axis, leading to immunosuppression. Little is known about other possible influences of PVN on immunomodulation. Evidence, however, has been accumulating recently, indicating possible involvement of other subnuclei of this nucleus. By using the c-fos technique, the present study investigated the neuronal groups of the PVN that were activated in response to intracerebroventricularly administered IL-1 beta. In addition to strong Fos expression in the dorsal part of medial parvocellular subnucleus of the PVN, where CRH neurons are located, two more neuronal groups were found to express Fos protein. One of which was the oxytocin-immunoreactive magnocellular neurons, mainly concentrated in the anterior and medial magnocellular subnuclei of the PVN. The magnocellular PVN subnuclei are known to project to, and release their hormones, in the posterior pituitary. Another group of Fos-immunoreactive neurons were found in the brainstem and spinal cord projecting area of the PVN. By combining retrograde tracing technique and Fos immunohistochemistry, it was proved that many of the spinal cord projecting PVN neurons were activated following IL-1 beta administration, through which the spinal cord sympathetic outflow might be regulated. The present study indicates that the hypothalamic PVN may serve as an integrative center for immunomodulation via three channels, i.e., the CRH and oxytocin neuroendocrinological and the PVN-spinal cord sympathetic neural channels.

Animals↗
PubMedDate not supplied

Direct morphological evidence of neuroimmunomodulation in colonic mucosa of patients with Crohn's disease.

Different neuropeptide-containing nerve fibers were investigated to clarify their role in the pathogenesis of Crohn's disease (CD) using immunohisto- and immunocytochemical techniques. Specimens were obtained from patients with CD from grossly affected colonic regions, from biopsies obtained from patients with CD treated with mesalazine and from control individuals. Quantitative analysis was made for the changes of the number of nerve terminals and their vesicle contents. The distribution pattern of all immunoreactive (IR) nerve fibers was similar both in the control and in the surgical specimens as well as in the biopsies obtained. The number of the synapses, the IR nerve fibers and their vesicle content were markedly decreased in the grossly affected colonic regions. Some degenerated axons were found in close proximity to the plasma cells. Immunocytochemistry demonstrated that substance P, vasoactive intestinal polypeptide and somatostatin IR nerve fibers were in direct contact with the plasma cells, lymphocytes and other immunocompetent cells. The gap between the membranes of immunoreactive nerve terminals and immunocompetent cells was 20-200 nm, in a few cases even less. In the mesalazine-treated group the number of the IR nerve terminals as well as their vesicle content was increased. These results suggest that changes in the number of different neuropeptide-containing nerve terminals and their content might alter the neuroimmunological processes, because these peptides are known to be immunoregulators.

Adolescent↗
PubMed2006

Healthy aging is associated with unaltered production of immunoreactive growth hormone but impaired neuroimmunomodulation.

BACKGROUND: Both endocrine and immune systems are continuously remodeled during aging. OBJECTIVE: Here, we investigated to what extent adrenal and somatosenescence are associated reciprocal changes in the immune system during strictly healthy aging. METHODS: Forty-six elderly subjects and 33 young adults were recruited according to the health criteria of the SENIEUR protocol. Peripheral blood mononuclear cells were isolated and stimulated in vitro with lipopolysaccharide or phytohemagglutinin to assess the production of immunoreactive growth hormone (GH). Peripheral sensitivity to steroids was assessed in vitro by dexamethasone-, cortisol- or dehydroepiandrosterone (DHEA)-induced inhibition of T-cell proliferation. DHEA and GH levels were measured by radioimmunoassays. RESULTS: Healthy elderly had lower salivary DHEA and serum GH levels (somatosenescence). They presented reduced T-cell sensitivity to dexamethasone but similar cellular sensitivities to cortisol and DHEA. Their cells produced similar levels of immunoreactive GH compared to the cells of young adults. CONCLUSIONS: These data indicate that healthy aging is associated with adrenal and somatosenescence as well as impaired neuroendocrine immunoregulation at the level of the lymphocyte. In addition, somatosenescence may not be associated with a reciprocal decline in immunoreactive GH.

Aged↗
PubMedDate not supplied

Neuroimmunomodulation in cancer patients: correlations between melatonin and beta-endorphin blood levels and T helper/suppressor ratio.

The pineal gland and opioid peptides play roles in the neuroendocrine control of immunity. Both neuroendocrine and immune dysfunctions have been observed in cancer but the importance of the altered secretion of neurohormones in the immunoincompetence of cancer patients has never been investigated. This study concomitantly evaluated neuroendocrine and immune functions in 40 patients with early or advanced neoplastic disease. In each patient, melatonin and beta-endorphin blood levels and lymphocyte subtypes were determined on venous blood samples collected during the morning. Metastatic patients had lower melatonin levels and a lower T4/T8 ratio than patients without metastases but no significant correlation was found between melatonin and the T4/T8 ratio. beta-endorphin levels appeared to be normal in all patients. These results suggest that melatonin and beta-endorphin secretion have no role in determining immune dysfunctions in cancer.

Adult↗
PubMed2001

Integrative neuroimmunomodulation of gastrointestinal function during enteric parasitism.

Enteric helminths have a significant impact on the structure, function, and neural control of the gastrointestinal (GI) tract of the host. Interactions between the host's nervous and immune systems redirect activity in neuronal circuits intrinsic to the gut into an alternative repertoire of defensive and adaptive motor programs. Gut inflammation and activation of the enteric neuroimmune axis play integral roles in the dynamic interaction between host and parasite that occurs at the mucosal surface. Three inter-related themes are stressed in this review to underscore the pivotal role that neural control mechanisms play in the host's GI tract functional responses to enteric parasitism. First, we address the discovery that signaling molecules of both parasite and host origin can reorient the dynamic ecology of enteric host-parasite interactions. Second, we explore what has been learned from investigations of altered gut propulsive and secretomotor reflex activities that occur during enteric parasitic infections and the emerging picture derived from these studies that elucidates how nerves help facilitate and orchestrate functional reorganization of the parasitized gut. Third, we provide an overview of the direct impact that enteric parasitism has on nerve cell function and neurotransmission pathways in both the enteric and central nervous systems of the host. In summary, this review highlights and clarifies the complex mechanisms underlying integrative neuroimmunophysiological responses to the presence of both invasive and noninvasive enteric helminths and identifies directions for future research investigations in this highly important but understudied area.

Animals↗
PubMedDate not supplied

Mechanisms involved in activation of human eosinophil exocytosis by substance P: an in vitro model of sensory neuroimmunomodulation.

Substance P (SP), a tachykinin with a wide range of biological activities including a priming effect on human eosinophil chemotaxis, was investigated for its influence on eosinophil cytotoxic function measured as degranulation of eosinophil-derived neurotoxin (EDN). Peripheral blood was obtained from healthy volunteers and the degranulation assays were performed using radioimmunoassay (RIA). SP and its C-terminal elicited EDN release in a time-dependent mode at a narrow range of doses with optimal activity of 10(-6) M. FK888 (NK-1 receptor antagonist) inhibited EDN release stimulated by SP in dose dependency, also a complete inhibition was observed when eosinophils were preincubated with 1000 ng/ml pertussis toxin (PTX). Pre-exposure of eosinophils to staurosporine resulted in blockage of SP-induced EDN release in a dose-dependent mode. On the other hand, SP at 10(-7) M and 10(-8) M primed eosinophils to suboptimal dose (10(-8) M) of Platelet activating factor (PAF) resulting into significant enhancement of EDN release. SP(4-11) fragment showed a similar activity while SP(1-4) fragment was not active. SP priming of eosinophils was not affected by Ca2+ depletion, however, it caused a change in the pattern of the intracellular calcium influx against the suboptimal dose of PAF. These results suggest that SP i) may induced human eosinophil matrix protein degranulation through a receptor mediated mechanism coupled to PTX sensitive G protein(s) with the probability of linkage to phospholipase C activation, and, ii) primes human eosinophils for an exalted inflammatory response through a Ca2+ independent pathway.

Calcium↗
PubMedDate not supplied

[Current concepts of neuroimmunomodulation].

Over the last decade, a considerable wealth of information has expanded and strengthened our knowledge of the relations between the nervous, endocrine, and immune systems. The following areas of progress may be underlined 1) the cells of the three systems appear to secrete similar substances and are sensitive to them, thus suppressing traditional differences between neurotransmitters, hormones and immune mediators; 2) new knowledge is available on hormone actions on the immune system, and direct and mutual influences between the nervous and the immune system have been documented; 3) brain areas selectively involved in immune regulation have been identified; 4) various brain functions are now known to be influenced by immune mediators; 5) neurological and psychiatric components have been described in autoimmune diseases. An immune etiology has been unraveled in a wide range of neural disorders. A neuroimmunological component has been documented in a growing number of diseases. Altogether, a new chapter is emerging in our understanding of homeostatic functions and their medical implications.

Animals↗
PubMed2001

[5-HT3 receptors in amygdala mediate neuroimmunomodulation in rats].

The present study was to explore the possible immunomodulatory role of 5-HT3 receptors in the amygdala in rats. Concanovalin A (Con A)- and lipopolysaccharide (LPS)-stimulated splenocyte proliferation response (SPR), production of IL-2, activity of natural killer (NK) cells and serum cortisol were measured by 3H-TdR incorporating method, MTT method and RIA, respectively. The Con A- and LPS-stimulated SPR was enhanced in a dose-dependent manner by 5-HT3 receptor antagonist granisetron (GNT) (0.1-0.4 mg/kg, i.p.). SPR was also enhanced by intracerebroventricular (icv) administration of 1-phenylbiguanide (PBG, 10 micrograms/d). Con A-stimulated SPR and production of IL-2 were increased either by bilateral or by unilateral central amygdala (CeA) microinfusion of PBG (0.5 microgram/side), but LPS-induced SPR and NK cell activity were not affected. On the contrary, the LPS-induced SPR was increased by either bilateral or unilateral basomedial amygdala (BmA) microinfusion of PBG (0.5 microgram/side). The plasma cortisol level was significantly raised by CeA or BmA PBG microinfusion, but the effect induced by PBG intra-CeA was greater than that induced by PBG intra-BmA (P < 0.01). The effects of icv PBG and intra-amygdala infusion were antagonized by granisetron. Asymmetrical modulation of immune reactivity by 5-HT3 receptors in CeA or BmA was not observed in these experiments. It is suggested that 5-HT3 receptors within the amygdala may modulate rat mitogen-stimulated SPR in different manners.

Amygdala↗