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Results for “Neuroimmunomodulation”

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PubMed1991

Evidence for immunomodulatory properties of prolactin in selected in vitro and in vivo situations.

The relationship between neuroendocrine regulation and the immune system has recently become the subject of intense investigations. The pituitary secretes both immunostimulatory (growth hormone and prolactin) and immunosuppressive (ACTH) hormones, and is thus involved in the control of immune functions. The present work was aimed at the study of the immunoregulatory properties of prolactin in selected in vitro and in vivo model situations. Prolactin was found to enhance recovery of the receptor for sheep red blood cells (in vitro). Compared with control cells, incubation with prolactin and/or prolactin containing sera significantly enhanced the capacity of trypsin treated lymphocytes from the peripheral blood of healthy volunteers to form E-rosettes. Chlorpromazine stimulated prolactin release in males, and lactation stimulated prolactin release in females raised the number of large granular lymphocytes in peripheral circulation. Sera containing elevated prolactin levels stimulated the metabolic activity of peripheral neutrophilic leukocytes. These results suggest that prolactin may stimulate selective functions of cellular immunity, and that it is involved in interactions between the nervous, the hormonal and the immune systems.

Adult↗

PubMed1991

Differential effect of beta-endorphin on three human cytotoxic cell populations.

We have examined in vitro the effect of the proopiomelanocortin gene product, beta-endorphin (bE), on the cytotoxic activity of natural killer (NK) cells, lymphokine activated killer (LAK) cells and cytotoxic T-lymphocytes (CTL). Our studies show that bE reproducibly suppressed LAK cytotoxic activity in all donors tested. The effect of bE on the generation of CTL varied, and was negligible on CTL cytotoxic function. Our study also confirms the variable nature of the effects of bE on NK cytotoxicity. In all instances, the effects of bE were generally small, but could be blocked by opioid receptor antagonists, or by prior heat-inactivation of the peptide. The magnitude of the effects was greatest at low effector:target ratios in all of the three systems studied. These results support the emerging body of evidence that the neuroendocrine system may influence host defense mechanisms mediated by cytotoxic cells.

Adolescent↗

PubMed1991

Association between circadian rhythms of endogenous hypothalamic opioid peptides and of natural killer cell activity.

To explore in man the hypothesis that natural killer cell activity and hypothalamic-hypophyseal hormones constitute a mutually coupled multioscillatory system, we analysed and compared, in 11 healthy volunteers, the circadian variations in plasma concentrations of beta-endorphin, met-enkephalin and alpha-MSH, and of natural killer activity of peripheral blood lymphocytes. Natural killer cell activity and plasma beta-endorphin levels showed a similar circadian rhythm with the peak in the morning (acrophases at 06.14 and 08.25, respectively), whereas the circadian rhythm of met-enkephalin was approximately in antiphase to the natural killer rhythm (acrophase close to 17,00 hours). Although daily variation of alpha-MSH showed greater inter-individual variability, a circadian rhythm was statistically validated. Analysis of correlation between rhythmometric parameters (mesor, amplitude, peak and nadir) of natural killer cell activity vs neuro-endocrine hormones revealed that the minimum and medium daily concentrations of beta-endorphin correlated directly with the corresponding parameters of natural killer activity, while the maximum and medium concentrations of met-enkephalin were inversely correlated with the peak and the mesor of natural killer activity. The amplitude of natural killer cell activity oscillations correlated directly with the peak, mesor and nadir concentrations of alpha-MSH. We show here that circadian rhythms of some neuroendocrine hormones of the hypothalamic-hypophyseal axis, i.e. beta-endorphin, met-enkephalin and alpha-MSH, are significantly coupled to daily oscillations of NK cell activity.

Adolescent↗

PubMed1993

Involvement of central opioidergic and nonopioidergic neuroendocrine systems in the suppressive effect of acupuncture on delayed type hypersensitivity in mice.

The effect of a single treatment of electroacupuncture (Acu) at early or late stages of the efferent phase on 2, 4, 6-trinitrochlorobenzene (TNCB)-induced delayed type hypersensitivity (DTH) was studied in intact and hypophysectomized (HPX) mice. Acu (2.5 Hz, 15 min) applied to the acu-point equivalent to GV4 at 0, 3, 18 or 21 h after TNCB challenge induced significant suppression (45-73%) of the maximal extent of ear swelling at 24 h after TNCB challenge. An immunosuppressive and antiinflammatory drug, prednisolone 10 mg/kg i.p., also suppressed the DTH to the same extent. Pretreatment with intracisternal injection of naloxone hydrochloride (2 micrograms) significantly blocked the Acu-evoked DTH suppression when Acu treatment was done at 0 or 3 h. On the contrary, naloxone did not block the effect of Acu treatment given at 21 h. In order to examine the potential involvement of the pituitary in the suppression of DTH by Acu, the DTH reaction was examined in HPX mice. Acu failed to produce suppressive response in the HPX mice unless given at 0 h. These findings indicate that Acu treatment at acu-point GV4 during the efferent phase of induced DTH can suppress the DTH through central opioidergic or nonopioidergic systems. The pituitary is apparently pivotal in this immunosuppression and it is suggested that the DTH suppression by Acu may be mediated via activation of the neuroendocrine system.

Animals↗

PubMed1993

Effect of stimulation on soluble proteolytic enzymes released by peripheral blood mononuclear cells.

The release of soluble peptidases active in the degradation of leucine enkephalin by human peripheral blood mononuclear cells (PBMC), and the effect of stimulation of mononuclear cells on the release of these enzymes are reported. Results obtained indicate that leu-enkephalin is partially degraded in the presence of soluble supernatants prepared from mononuclear cells. In accord with data previously obtained with immunocompetent cell lines, three classes of enzymes appear to be involved in leu-enkephalin hydrolysis: aminopeptidases, dipeptidylaminopeptidases and dipeptidylcarboxypeptidases. Phytohemagglutinin stimulation of mononuclear cells appears to cause a relevant increase of the total activity of the soluble enzymes, as well as a partial rearrangement of the ratio between the different enzyme activities. A similar effect is also evident upon chromatographic separation of the soluble supernatants: the relative activity of the several distinct enzymes--notably aminopeptidases and dipeptidylaminopeptidases--identified after column separation is significantly modified by PBMC stimulation. The effect of stimulation of mononuclear cells on the release of soluble enzymes can be interpreted as an indication of the role of these enzymes--possibly in the regulative process of informational peptides--similar to that described in the case of membrane enzymes.

Amino Acid Sequence↗

PubMed1995

Mechanisms of conditioned immunomodulation.

This article presents some recent work from our laboratory indicating that multiple physiological systems play a role in conditioned immunomodulation. The first study shows that naltrexone, but not N-methylnaltrexone, blocks the suppressive effects of an aversive conditioned stimulus on Con-A-induced proliferation and natural killer cell activity of splenic lymphocytes. This finding indicates that central opioid activity is involved in the conditioned effects. The second study shows that the beta-adrenergic antagonists atenolol and ICI-118,551 block of the suppressive effects of an aversive conditioned stimulus on Con-A-induced proliferation, but have no effect on natural killer cell activity. This result indicates the involvement of the adrenergic system in a subset of the conditioned effects. Collectively, these experiments provide evidence that both the opioid system and the sympathetic nervous system are involved in conditioned immunomodulatory changes elicited by an aversive conditioned stimulus.

Animals↗

PubMed1996

Positive and negative immunomodulation by opioid peptides.

The data that follow review part of the existing evidence concerning the neuroimmune functions mediated by opioid peptides, with particular regard to dual immunomodulatory effects. Limited references to substances other than opioid peptides are included, mainly to emphasize the possible similarities in the mediation of neuroimmune interactions by different informational substances, while the interactions directed from the immune to the nervous system have deliberately been omitted.

Adjuvants, Immunologic↗

PubMedDate not supplied

The neuroimmunology of stress from invertebrates to man.

Stress can be seen as the body's most important and complex reaction to ensure survival involving the neuroendocrine systems and a variety of other organs. The investigation of the evolutionary bases of stress argues that the basic mechanisms and molecules involved in stress (CRH, ACTH, glucocorticoids, biogenic amines and cytokines) are fundamentally similar and well preserved throughout evolution in different species and taxa. A review of available data highlights that the involvement of immunity during stress response has a strong evolutionary basis and is not a mere consequence of glucocorticoid hormone release. We propose that the evolutive cellular bases of stress are to be identified in immune cells, such as invertebrate hemocytes, producing a variety of cytokine-like molecules, capable at the same time of producing a variety of hormone- and neuropeptide-like molecules and of performing a proto-stress response (release of biogenic amines). We conclude that stress, a highly conserved reaction remarkably similar in different species and taxa, is a fundamentally positive type of adaptive reaction.

Animals↗

PubMed1993

Prolactin receptor expression by lymphoid tissues in normal and immunized rats.

Prolactin receptor (PRLr) expression and distribution in thymus, spleen, bone marrow, lymph nodes, and peripheral blood lymphocytes from young adult Lewis rats are analyzed using single-color flow cytometry and a well-characterized monoclonal antibody directed against the rat liver PRLr. The in vivo effects of regional immunization on PRLr expression are also examined. PRLr is found to be widely distributed among cells of the immune system and demonstrates lymphoid tissue-specific patterns of expression. Footpad immunization caused the rapid, but transient, induction of PRLr expression in the draining lymph node, with only modest effects on PRLr expression in other distant lymphoid tissues. These studies indicate that PRL may be capable of direct interaction with the immune system through differential expression of the PRL cell surface receptor on select lymphoid target cell populations.

Animals↗

PubMed1993

On the potential role of proopiomelanocortin in skin physiology and pathology.

Pro-opiomelanocortin (POMC) is the precursor of ACTH, alpha-MSH and beta-endorphin, neuropeptides with multiple regulatory functions. Both the pituitary gland and peripheral tissues such as mammalian skin are capable of generating POMC-derived neuropeptides. Mammalian skin is also a target for POMC products; their possible roles in skin physiology and pathology are discussed in this communication.

Amino Acid Sequence↗

PubMed1991

Neuroimmunomodulatory effects of acupuncture in mice.

The purpose of this study was to assess the effect of acupuncture on the immunological response. The induction of anti-sheep red blood cells (SRBC) plaque-forming cells (PFC) was used as a measurement of the immune response to treatment. In normal non-immunized mice, enhancement of PFC was seen after a single acupuncture treatment when spleen cells from stimulated mice were cultured with SRBC in vitro. After 3 acupuncture treatments, spleen cells from mice did not show PFC enhancement after treatment with anti-Thy-1.2 antibody and complement, nor after the removal of non-adherent cells. Serum obtained from mice 1 h after acupuncture stimulation enhanced the PFC of normal spleen cells in vitro, but the enhancement was abolished by the addition of propranolol. These results suggest that acupuncture, by activation of the autonomic nervous system, modulates the immune response.

Acupuncture Therapy↗

PubMed1994

Modulation of immune reactivity by unilateral striatal and mesolimbic dopaminergic lesions.

Asymmetrical modulation of immune reactivity by central dopaminergic pathways was suggested by previous reports which described an association between alterations of immune response and peculiar patterns of dopamine asymmetries in pathological and physiological situations. In the present experiments, we studied the respective roles of the nigrostriatal and mesolimbic dopaminergic networks in the asymmetrical modulation of immune responses. Lymphocyte proliferation as well as natural killer (NK) cell activity were analysed in mice, 2 weeks after unilateral lesions of dopaminergic projections by in situ injection of 6-hydroxydopamine in the striatum or the nucleus accumbens. After lesions of the striatum, proliferation of splenic lymphocytes was impaired only in the right-lesioned group. Left-lesions appeared to not modify T lymphocyte reactivity. After lesions of the nucleus accumbens, no modification of T lymphocyte mitogenesis was observed but splenic NK cell activity was depressed in left-lesioned mice as compared with controls or right-lesioned animals. Proliferation of B lymphocytes was not affected by striatal or mesolimbic dopaminergic lesions. It was concluded that both striatal and mesolimbic dopaminergic pathways are asymmetrically involved in neuro-immunomodulation. These dopaminergic regions appear to function independently as the effective side as well as the immune parameters that were altered differ according to the structure lesioned.

Animals↗

PubMed1990

Alcohol withdrawal syndrome--an auto-immune disease? A neuroimmunologic model for pathogenesis of alcohol withdrawal symptoms.

A neuroimmunologic model of alcohol withdrawal symptoms is developed according to which these may be considered as an idiopathic auto-immune disease. During the alcohol abuse period of non-addicts, homeostasis may alter pathologically by gradual adaptation of the organism: auto-sensitisation develops and finally leads to the breakdown of auto-immune tolerance of the structural modifications set by alcohol withdrawal. The immunosystem regards the existing assimilation of alcohol as self, the withdrawal of alcohol as non-self. Alcohol withdrawal may be considered as an acknowledged physical stressor, and physical stressors as potential triggers of auto-immune diseases. Some so-called alcohol-induced diseases may originate in the pathogenic effects of preceding auto-immune responses to repeated alcohol withdrawals. Neuroimmunologic preconditions of potential auto-immune diseases exactly fit the alcohol withdrawal situation. Neuroimmunologic diseases themselves show close analogies respectively to alcohol withdrawal symptoms as well as to some alcohol-induced diseases. The myelin basis protein is assumed to be a potential auto-allergen. Finally withdrawal symptoms being the expression of physical dependence on alcohol, the model may highlight the very nature of physical dependence.

Autoimmune Diseases↗

PubMed1991

Does prolactin play a role in skin biology and pathology?

Despite its extensive repertoire of biological activities, which include the growth- and osmoregulation of epithelial tissues as well as immunoregulatory properties, the potential significance of the pituitary hormone prolactin (PRL) for human skin biology and pathology has yet to be fully appreciated. In this essay, the hypothesis is presented that PRL acts as a neuroendocrine modulator of skin epithelial cell proliferation and of the skin immune system by forming a 'prolactin-circuit' between the central nervous system and the skin. Binding to specific skin receptors, modulation of cytokine release in the skin, and stimulation of somatomedin release by mesenchymal cells are among the suggested pathways by which PRL could affect epithelial cell growth in the skin. Potential feedback signals, arising from the skin and modifying pituitary PRL release, are briefly outlined. Centering on the role of PRL in both psoriasis and hair growth as models for studying the proposed PRL-skin connection, clinical and experimental evidence in support of this theory is discussed in the context of a 'neuroimmune-dermatological' perspective.

Central Nervous System↗

PubMed1995

A new approach to antiviral therapy.

A new approach to antiviral therapy is proposed, taking advantage of the recently investigated innervation of immune tissues by the sympathetic nervous system, which establishes a functional connection between the nervous and the immune system, where the sympathetic nervous system exerts a varying tonic inhibitory influence on cellular activation via secretion of norepinephrine and reception thereof by beta-receptors on leukocytes. Simultaneous beta-adrenergic blockade of leukocytes and stress-related centres of the central nervous system (paraventricular nucleus of the hypothalamus) is suggested as immunoactivating therapy in presence of foreign antigen. Immunoactivation is newly defined as facilitated activation of the immune system in presence of foreign antigen and is theoretically correlated with indirect antiviral and antitumoral activity.

Adjuvants, Immunologic↗

PubMed1996

Biphasic changes in behavioral, endocrine, and sympathetic systems in adjuvant arthritis in Lewis rats.

Adjuvant arthritis (AA) is an experimental model for rheumatoid arthritis, and is induced most easily in inbred Lewis rats by an intradermal injection of heat-killed Mycobacterium tuberculosis (MT) in incomplete Freund's adjuvant. Susceptivity to the arthritis in Lewis rats is thought to be related to a defect in their responses of the hypothalamo-pituitary-adrenal (HPA) axis to the disease. Because the use of an inbred strain is necessary for our immunological studies, we examined in Lewis rats changes in behavior, the HPA axis, and sympathetic nerve activities during development of the adjuvant arthritis. Following intradermal injections of heat-killed MT in adjuvant, the arthritis began to develop on day 12, reaching its maximum severity on day 21, and remained at the level for over a month. The body temperature rose from day 0 to 5 (the primary phase--before the onset of the arthritis). It then fell to normal temperature, and again rose from day 10 to 21 (the secondary phase--with fully developed arthritis). The behavioral (physical activity, food, and water intake) and hormonal parameters [plasma adrenocorticotropic hormone (ACTH) and corticosterone levels] also changed in two phases, similar to those observed in the temperature responses. No change in plasma vasopressin level was observed. Sympathetic nerve activities, assessed by changes in plasma noradrenalin levels, increased more in the primary than in the secondary phase. The possible causes for the biphasic changes associated with development of arthritis are discussed.

Animals↗

PubMed1996

Effects of nerve growth factor on splenic norepinephrine and pineal N-acetyl-transferase in neonate rats exposed to alcohol in utero: neuroimmune correlates.

Prenatal alcohol exposure (FAE) has been associated with multiple anomalies, including a selective developmental delay of sympathetic innervation in lymphoid organs. Sympathetic neurons require nerve growth factor (NGF) for their development and maintenance, and recent evidence has suggested that alcohol impairs the synthesis and/or biological activity of NGF in selected central and peripheral neurons. Thus, the present study examined the hypothesis that NGF administration to FAE rats during early postnatal development would reverse some of the peripheral sympathetic deficits. Neonate rats, FAE and the corresponding control cohorts, received daily treatments of NGF or cytochrome C (0.3 mg/kg; s.c.) for various time intervals, and were killed 24 hr or 10 days after the last treatment. The measured parameters included norepinephrine (NE) concentrations in the spleen and heart, which receive nor-adrenergic innervation from the coeliac ganglion and the superior cervical ganglion (SCG), respectively. In addition, we measured the activity of pineal N-acetyltransferase (NAT), the rate-limiting enzyme of melatonin biosynthesis, which depends on sympathetic innervation from the SCG. The data show that chronic, but not acute, NGF treatments reversed the FAE-related deficits in splenic NE concentrations as well as in pineal NAT activity in a time- and age-dependent manner. Sympathetic neurons play an important role in immune modulation. Thus, the altered splenic NE levels and pineal NAT activity may play a role in immune deficits associated with exposure to alcohol in utero.

Animals↗

PubMed1988

Altered cerebral dominance in an atopic population.

Handedness was assessed in 853 subjects, 424 from an allergy office practice and 429 from a health screening clinic, using a modified Oldfield Handedness Inventory. Subjects also responded to a survey ascertaining both personal and family histories of allergy-related problems and left-handedness. A significant left-handed shift in mean laterality quotient and an increased incidence of left-handedness was found in participants from the allergy office and in subjects who considered themselves to be affected by allergy, allergic rhinitis, and/or asthma. Controlling for nonatopic responders from the allergy office and possibly atopic responders from the health screening clinic, mean laterality quotients were 66.4 +/- 51.6 vs 79.4 +/- 42.1 (p less than .001) and the incidence of left-handedness was 12.1% vs 6.8% (p less than .05). Mean laterality quotient of 125 asthmatics was 65.1 +/- 54.0, and 16 (12.8%) were left-handed. The mean percentage of left-handed children of 79 asthmatic parents was found to be increased: 16.7 +/- 26.3% vs 10.3 +/- 21.2% of children of 198 nonatopic parents (p less than .02). This was attributable to left-handed children of asthmatic women, 18.6 +/- 29.0% (p less than .01), but not asthmatic men. Both autonomic neurologic dysfunction and disordered immunoregulation typify atopic disease. Our results can be interpreted to reflect this duality and lend support to Geshwind's hypothesis of a relationship between cerebral dominance and immunologic set resulting from common developmental influences.

Adult↗