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Results for “Behavioral immune system”

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PubMed1998

Brain NPY Y1 receptors rapidly mediate the behavioral response to novelty and a compartment-specific modulation of granulocyte function in blood and spleen.

Neuropeptide Y (NPY) alters behavioral activity and innate immune functions of rats within minutes of intracerebroventricular (i.c.v.) application. Using combinations of the Y1-5a,b(6) agonist NPY, the Y1,3,5 agonist [Leu31-Pro34]NPY (LP-NPY), and the selective Y1 antagonist BIBP3226 (BIBP), we investigated whether the NPY-Y1 receptor (Y1R) subtype regulates NPY-induced behavioral and immunological effects at 15 min after i.c.v. application. Administration of both NPY and LP-NPY decreased rearing activity in the open field and suppressed granulocyte function in the blood. These effects were blocked by BIBP pre-treatment. In contrast to the blood, NPY and BIBP+NPY treatments stimulated granulocyte function within the splenic compartment. In addition, a blood leukophilia composed of granulocytes and NK cells was induced by NPY only. We conclude that the tested early effects of NPY are mediated by either the Y1R (rearing, blood granulocyte function), or a non-Y1R (splenic granulocyte function), or by a combined receptor activation (leukocyte mobilization). Furthermore, the immunological effects of NPY demonstrate compartment specificity.

Animals↗
PubMed1989

Psychoneuroimmunology for the psychoneuroendocrinologist: a review of animal studies of nervous system-immune system interactions.

Evidence for interactions between the nervous and immune systems arises from a number of experimental observations: the behavioral conditioning of immune responses, the effects of stimulation or lesion of brain sites on immune system function, the effects of stressors on immune responses and tumor growth, and physiological and neurochemical changes in the brain during immune responses. The links between the nervous and immune systems probably include glucocorticoids secreted from the adrenal gland, catecholamines and neuropeptides secreted by sympathetic terminals and the adrenal medulla, certain pituitary and gonadal hormones, and polypeptides produced by cells of the immune system. The effect of glucocorticoids is not exclusively immunosuppressive, nor is it adequate to explain all the effects of stress. The effects of opiates on immune function are complex; in vitro, endogenous opiates most often facilitate immune activity, but in vivo, opiates appear to inhibit immune responses and impair tumor rejection. The in vitro effects are rarely prevented by naloxone pretreatment and appear to require the integrity of the C- rather than the N-terminal of beta-endorphin, suggesting a nonopiate character. Infections or the administration of antigens increase circulating concentrations of glucocorticoids and activate cerebral catecholaminergic metabolism, especially in the hypothalamus. These responses suggest that challenges to the immune system are physiologic stressors. Interleukin-1 (IL-1) produced by immune cells may be the mediator of these effects, thus acting as an "immunoneurotransmitter". The cerebral responses suggest that the brain can monitor the progress of immune responses. IL-1 and the glucocorticoids together may form a regulatory feedback mechanism for immune responses.

Animals↗
PubMed2002

Behavioral conditioning of immunosuppression is possible in humans.

Behavioral conditioned immunosuppression has been described in rodents as the most impressive demonstration of brain-to-immune system interaction. To analyze whether behavioral conditioned immunosuppression is possible in humans, healthy subjects in this double-blind, placebo-controlled study were conditioned in four sessions over 3 consecutive days, receiving the immunosuppressive drug cyclosporin A as an unconditioned stimulus paired with a distinctively flavored drink (conditioned stimulus) each 12 h. In the next week, re-exposure to the conditioned stimulus (drink), but now paired with placebo capsules, induced a suppression of immune functions as analyzed by the IL-2 and IFN-gamma mRNA expression, intracellular production, and in vitro release of IL-2 and IFN-gamma, as well as lymphocyte proliferation. These data demonstrate for the first time that immunosuppression can be behaviorally conditioned in humans.

Adult↗
PubMed2002

Psychoneuroimmunology: new avenues of research for the twenty-first century.

Psychoneuroimmunology (PNI) investigates the relations between the psychophysiological and immunophysiological dimensions of living beings. PNI brings together researchers in a number of scientific and medical disciplines, including psychology, the neurosciences, immunology, physiology, pharmacology, psychiatry, behavioral medicine, infectious diseases, and rheumatology. All are scientists with profound interest in interactions between the nervous and immune systems, and the relation between behavior and health. Despite the variety in domains and approaches to research, the outcome common to all research endeavors is the discovery of new information, of uncovered facts, of novel evidence, which contributes to the continuing generation of knowledge. In this paper we discuss psychoneuroimmune aspects of some conditions that are not routinely immediately associated with immunity, such as the condition of being the caregiver of somebody suffering from dementia; the effect on the brain-body modulations of aluminum, a metal that is not a component of the human body; and insomnia, a fairly common but disturbing disease, that even today lacks an effectual treatment.

Aluminum↗
PubMed2002

The concept of sickness behavior: a brief chronological account of four key discoveries.

Neurons do not have receptors to detect bacteria or viruses, yet the presence of these microorganisms can cause a sickness behavior syndrome that includes, e.g., fever, anorexia, and lethargy. Because the immune system has receptors capable of detecting these non-cognitive stimuli, how the immune system transmits a message to the brain has been studied to understand why behavior is altered in sick animals. The focus has been on several cytokines secreted by leukocytes; these include interleukin (IL)-1beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha). These cytokines are secreted by activated mononuclear phagocytic cells, and numerous studies show that both peripheral and central injection of IL-1beta, IL-6, and TNF-alpha induce sickness behavior. Moreover, these cytokines and their receptors are present in the brain and inhibiting the secretion of cytokines or blocking their receptors in the brain blocks or abrogate the behavioral responses induced by inflammatory stimuli. Because the sickness behavior syndrome modulates the immune system and enhances recovery, the interplay between the immune system and central nervous system is an essential part of the overall host defense against pathogenic microorganisms. The purpose of this brief paper is to provide a chronological description of four critical advances that have led to the current understanding of how the immune system communicates with the brain to induce sickness behavior. Results from several key studies will be discussed, which showed that: (1) sickness behavior is a motivational state; (2) sickness behavior is a well-organized adaptive response to infection; (3) cytokines produced by activated leukocytes induce sickness behavior; and (4) cytokines transmit messages from the periphery to the brain using humoral and neural pathways.

Adaptation, Physiological↗
PubMed2005

Behavioral, endocrine and immunological characteristics of a murine model of premature aging.

We have previously shown that differences in life span among members of Swiss mouse populations appear to be related to their exploration of a T-maze, with a slow exploration ('slow mice') being linked to alteration of spontaneous behavior and monoaminergic systems, impaired immune function and shorter life span. In general these traits resemble some of the characteristics of chronologically old animals. Thus, we proposed the 'slow mice' as a model of prematurely aging mice (PAM). Now, we have compared female PAM with non-prematurely aging mice (NPAM) as regards a number of behavioral, endocrine and immunological parameters which were studied under both basal and stress conditions. In the present study the animals were chronologically younger than those used in our previous work. When compared to NPAM, the PAM showed increased anxiogenic-like responses in the plus-maze, increased basal corticosterone levels and decreased corticosterone responses to stress. The PAM also showed a decreased natural killer activity as well as decreased lymphoproliferative responses to mitogens. Moreover, the mitogen-induced lymphoproliferative responses of the PAM appeared to be more susceptible to stress. The data indicate that certain characteristics of the PAM are already present in animals of very young chronological age and provide new information for a more complete characterization of the PAM from a neuroimmunoendocrine viewpoint.

Age Factors↗
PubMed1998

Illness from low levels of environmental chemicals: relevance to chronic fatigue syndrome and fibromyalgia.

This article summarizes (1) epidemiologic and clinical data on the symptoms of maladies in association with low-level chemicals in the environment, i.e., environmental chemical intolerance (CI), as it may relate to chronic fatigue syndrome (CFS) and fibromyalgia; and (2) the olfactory-limbic neural sensitization model for CI, a neurobehavioral synthesis of basic and clinical research. Severe CI is a characteristic of 20-47% of individuals with apparent CFS and/or fibromyalgia, all patients with multiple chemical sensitivity (MCS), and approximately 4-6% of the general population. In the general population, 15-30% report at least minor problems with CI. The levels of chemicals reported to trigger CI would normally be considered nontoxic or subtoxic. However, host factors--e.g., individual differences in susceptibility to neurohormonal sensitization (amplification) of endogenous responses--may contribute to generating a disabling intensity to the resultant multisystem dysfunctions in CI. One site for this amplification may be the limbic system of the brain, which receives input from the olfactory pathways and sends efferents to the hypothalamus and the mesolimbic dopaminergic [reward] pathway. Chemical, biologic, and psychological stimuli can initiate and elicit sensitization. In turn, subsequent activation of the sensitized limbic and mesolimbic pathways can then facilitate dysregulation of behavioral, autonomic, endocrine, and immune system functions. Research to date has demonstrated the initiation of neurobehavioral sensitization by volatile organic compounds and pesticides in animals, as well as sensitizability of cardiovascular parameters, beta-endorphin levels, resting EEG alpha-wave activity, and divided-attention task performance in persons with CI. The ability of multiple types of widely divergent stimuli to initiate and elicit sensitization offers a new perspective on the search for mechanisms of illness in CFS and fibromyalgia with CI.

Controlled Clinical Trials as Topic↗
PubMedDate not supplied

[Behavior-immunity relationship: the role of cytokines].

There are several phenomena in which the immune and the central nervous systems regulate each other. However, their mechanisms are poorly understood. Since cytokines have a central role in the regulation of the immune response, this review describes their participation in two forms of neuro-immune communication, immunomodulation by psychological stress and behavioral conditioning of immune response. The role of cytokines in the endocrine and behavioral effects of acute phase, where cytokines have an effect in functions of the central nervous system, is also reviewed. The effects of psychological stress are described as both immunosuppressing and immunoenhancing. Among them, a relevant immunosuppressing one is the reduction of IL-1, IL-2, and IFN-gamma levels. In contrast, some of the pro-inflammatory effects of stress are mediated by an increase in the levels of IL-6, IL-1, and TNF mediated by the neurotransmitter Substance P. A possible role for IL-1 and IFN-beta as possible messengers in immune regulation by behavioral conditioning is proposed. Pro-inflammatory cytokines in turn can activate the hypothalamus-pituitary-adrenal axis and induce sickness behavior during the acute phase response, during which the parasympathetic nervous system serves as pathway for their detection by the central nervous system. An account is given about recent findings on the regulation of cytokine expression by neurotransmitters from the sympathetic nervous system (epinephrine and norepinephrine), a key piece in all these mechanisms of brain-immune communication. Possible mechanisms and pathways of communication between the brain and the immune system, as well as the possible participation of other cytokines are discussed.

Animals↗
PubMed1998

Brain type I but not type II IL-1 receptors mediate the effects of IL-1 beta on behavior in mice.

In the immune system, interleukin (IL)-1 beta effects are mediated by the type I IL-1 receptors (IL-1RI), whereas the type II IL-1 receptors (IL-1RII) act as inhibitory receptors. IL-1RI and IL-1RII are also present in the brain. To study their functionality in the brain, mice were centrally treated with neutralizing monoclonal antibody (MAb) directed against IL-1RI (35F5, 1 microgram) or against IL-1RII (4E2, 2 micrograms) and were centrally injected with recombinant rat IL-1 beta at a dose (2 ng) that decreased social exploration. Only 35F5 was effective in abrogating the behavioral effect of IL-1 beta. Moreover, 4E2 (1 microgram i.c.v.) did not potentiate the behavioral response to a subthreshold dose of IL-1 beta (1 ng i.c.v.). To examine the ability of brain IL-1RI to mediate the effects of endogenous IL-1 beta, mice were centrally treated with 35F5 (4 micrograms) and peripherally injected with IL-1 beta (1 microgram). Like IL-1 receptor antagonist (4 micrograms i.c.v.), 35F5 abrogated the effects of IL-1 beta. These results suggest that brain IL-1RI mediates the behavioral effects of IL-1 beta in mice.

Animals↗
PubMedDate not supplied

Cannabinoid exposure: effects on development.

The literature concerning the teratologic effects of cannabinoids is reviewed, and some methodological issues associated with perinatal cannabinoid exposure are discussed. The long-term consequences of perinatal cannabinoid exposure on brain, endocrine, immune, and hepatic functions are considered. In our studies, perinatal cannabinoid exposure affected the long-term development of body weight regulation, neuroendocrine function, and adult sexual behaviors. In addition, the immune system and hepatic cytochrome P-450 levels were also influenced in adult male mice perinatally-exposed to cannabinoids. It is hypothesized that these effects may be mediated by cannabinoid-induced alterations in the fetal and/or neonatal hormonal milieu. In addition, the possibility that perinatal cannabinoid administration affects the subsequent ability of the exposed offspring to adapt to the environment is discussed. Finally, possible mechanisms of cannabinoid action in altering development are evaluated. It is concluded that the evidence to date indicates that cannabinoids can be embryocidal, affect gestational length and labor, induce maturational delays, and that these substances affect a myriad of physiological processes in the developing offspring, including effects on behavioral parameters, not only in laboratory animals, but also in the human neonate. Consequences of perinatal cannabinoid exposure on development are described and possible mechanisms of action of cannabinoids are discussed.

Abnormalities, Drug-Induced↗
PubMed2005

The olfactory bulbectomised rat as a model of depression.

Bilateral olfactory bulbectomy results in changes in behavior, and in the endocrine, immune and neurotransmitter systems, that simulates many of those seen in patients with major depression. The olfactory system in the rat forms a part of the limbic region in which the amygdala and hippocampus contribute to the emotional and memory components of behavior. However, the loss of olfaction alone, which results from bulbectomy, is not the major factor that contributes to the behavioral abnormalities as peripherally induced anosmia does not cause the same behavioral changes. Thus it would appear that bulbectomy causes a major dysfunction of the cortical-hippocampal-amygdala circuit that underlies the behavioral and other changes. These neuroanatomical areas also seem to be dysfunctional in the patient with major depression. Chronic, but not acute, administration of antidepressants largely corrects most the behavioral, endocrine, immune and neurotransmitter changes that occur following bulbectomy. Thus the olfactory bulbectomized rat is not only a model for detecting antidepressant activity but also one for exploring the inter-relationships between these systems that are also dysfunctional in patients with major depression.

Animals↗
PubMed1996

Regulation of tumor growth and metastasis by thrombospondin-1.

Thrombospondin-1 (TSP1) is an extracellular matrix glycoprotein that influences cell adhesion, motility, and growth. Based on its effects on tumor and endothelial cell behavior, this member of the thrombospondin gene family has attracted interest as a potential regulator of tumor growth and metastasis. Initial studies have confirmed that increased TSP1 expression suppresses growth or metastasis of some tumors in vivo and inhibits angiogenesis. These activities are cell type specific, however, since overexpression of TSP1 in some tumors causes increased tumor progression. One basis for these apparently conflicting observations may be the complexity of the protein. TSP1 interacts specifically with several cell-surface receptors, heparan sulfate proteoglycans, growth factors, and other matrix components. These multiple binding specificities, combined with the ability of TSP1 to activate latent transforming growth factor beta and inhibit several proteases, suggest that exposure to TSP1 may initiate several intracellular signals. The integration of these signals may allow varied responses to TSP1. Furthermore, these signals may be received by the tumor cells, endothelial cells responsible for neovascularization, stromal cells, or cells of the host immune system. TSP1 influences specific behaviors of each cell type. Relating these phenomena to the molecular interactions of TSP1 observed in vitro may lead to novel therapeutic strategies for controlling cancer progression and metastasis.-Roberts, D. D. Regulation of tumor growth and metastasis by thrombospondin-1.

Amino Acid Sequence↗
PubMed1998

Cytokines for psychologists: implications of bidirectional immune-to-brain communication for understanding behavior, mood, and cognition.

The brain and immune system form a bidirectional communication network in which the immune system operates as a diffuse sense organ, informing the brain about events in the body. This allows the activation of immune cells to produce physiological, behavioral, affective, and cognitive changes that are collectively called sickness, which function to promote recuperation. Fight-flight evolved later and coopted this immune-brain circuitry both because many of the needs of fight-flight were met by this circuitry and this cooptation allowed the immune system to respond to potential injury in anticipatory fashion. Many sequelae of exposure to stressors can be understood from this view and can take on the role of adaptive responses rather than pathological manifestations. Finally, it is argued that activation of immune-brain pathways is important for understanding diverse phenomena related to stress such as depression and suppression of specific immunity.

Affect↗
PubMed1990

Neurobehavioral and immunological effects of prenatal cocaine exposure in rat.

Time-pregnant Sprague-Dawley rats were injected subcutaneously with 20 mg/kg of cocaine HCl or 0.9% saline daily from gestation days 15 through 21. Maternal plasma levels of approximately 720 ng/ml of cocaine did not alter maternal weight gain during treatment, duration of pregnancy, any of the litter variables or several indices of maternal behavior. Offsprings' body weight from birth to 30 days of age and physical maturation were not generally affected by prenatal cocaine exposure. While the development of surface righting, cliff avoidance, and the startle response was accelerated in cocaine-exposed offspring, acquisition of a preference for a social odor was unaltered. Prenatal cocaine also attenuated the locomotor response of the offspring to d-amphetamine and cocaine at PND 15; at PND 30 both of these catecholaminergic agonists increased activity in prenatal saline and prenatal cocaine offspring. However, the difference in plasma levels of cocaine at PND 30 suggests a possible down-regulation of adrenergic receptors following prenatal cocaine exposure. Decreased thymus/body weight ratios and splenomegaly were observed in prenatal cocaine animals at 55 days of age. Although complete neutralization of herpes simplex virus-type 1 was not observed, sera from prenatal cocaine offspring showed an increased rate of appearance of cytopathic effect, while sera from animals given cocaine postnatally showed a reduction in the rate at which viral infectivity was expressed in culture. These results indicate that prenatal cocaine exposure can alter neurobehavioral ontogeny and humoral immune responsitivity in the offspring.

Animals↗
PubMed1995

Natural tolerance in a simple immune network.

The following basic question is studied here: In the relatively stable molecular environment of a vertebrate body, can a dynamic idiotypic immune network develop a natural tolerance to endogenous components? The approach is based on stability analyses and computer simulation using a model that takes into account the dynamics of two agents of the immune system, namely B-lymphocytes and antibodies. The study investigates the behavior of simple immune networks in interaction with an antigen whose concentration is held constant as a function of the symmetry properties of the connectivity matrix of the network. Current idiotypic network models typically become unstable in the presence of this type of antigen. It is shown that idiotypic networks of a particular connectivity show tolerance towards auto-antigen without the need for ad hoc mechanisms that prevent an immune response. These tolerant network structures are characterized by aperiodic behavior in the absence of auto-antigen. When coupled to an auto-antigen, the chaotic attractor degenerates into one of several periodic ones, and at least one of them is stable. The connectivity structure needed for this behavior allows the system to adopt particular dynamic concentration patterns which do not lead to an unbounded immune response. Possible implications for the understanding of autoimmune disease and its treatment are discussed.

Animals↗
PubMed2005

A coherent framework for multiresolution analysis of biological networks with "memory": Ras pathway, cell cycle, and immune system.

Various biological processes exhibit characteristics that vary dramatically in response to different input conditions or changes in the history of the process itself. One of the examples studied here, the Ras-PKC-mitogen-activated protein kinase (MAPK) bistable pathway, follows two distinct dynamics (modes) depending on duration and strength of EGF stimulus. Similar examples are found in the behavior of the cell cycle and the immune system. A classification methodology, based on time-frequency analysis, was developed and tested on these systems to understand global behavior of biological processes. Contrary to most traditionally used statistical and spectral methods, our approach captures complex functional relations between parts of the systems in a simple way. The resulting algorithms are capable of analyzing and classifying sets of time-series data obtained from in vivo or in vitro experiments, or in silico simulation of biological processes. The method was found to be considerably stable under stochastic noise perturbation and, therefore, suitable for the analysis of real experimental data.

Algorithms↗
PubMed2004

Postirradiation volatile secretions of mice: syngeneic and allogeneic immune and behavioral effects.

The immune response in immunologically and olfactorily high- and low-reactive CBA and C57Bl/6 mice is almost similarly decreased after exposure to volatile secretions of syngeneic animals exposed to ionizing radiation in a dose of 4 Gy. In the preference/avoidance test intact animals prefer secretions of irradiated syngeneic and allogeneic animals to those of intact animals, while without irradiation animals of both strains prefer syngeneic secretions. C57Bl/6 mice differ from CBA animals by lower sensitivity.

Animal Communication↗