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Results for “Behavioral immune system”

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PubMed1990

Passive avoidance behavior, vasopressin and the immune system. A link between avoidance latency and immune response.

The relation between passive avoidance behavior and primary antibody response was studied in rats. The avoidance latency was varied by means of variation of the shock intensity during the learning trial; a higher shock intensity resulted in a longer avoidance latency at the retention test. The avoidance latencies were inversely proportional to the magnitude of the primary antibody response. Neuropeptides, such as [Arg8]-vasopressin (AVP) were shown to potentiate retrieval processes. Administration of 10 ng desglycinamide AVP (DGAVP) 1 h prior to the retention test facilitated passive avoidance behavior (increase in avoidance latency). Conversely i.c.v administration of vasopressin antiserum resulted in attenuation of the avoidance behavior. The effects of altered passive avoidance behavior as a consequence of i.c.v. administration of DGAVP or vasopressin antiserum were studied on the primary antibody response. Again an inversely proportional relationship between the avoidance latency and the magnitude of the primary antibody response was observed. The results show that the immune system can specifically react to graded environmental stimuli. It is hypothesized that vasopressin may be an endogenous mediator determining the outcome of the avoidance behavior and the primary antibody response.

Animals↗
PubMed1999

Reproductive phenotypes in the estrogen receptor-alpha knockout mouse.

The generation and initial characterizations of the ER alpha KO and has proved exciting, however, it is worth noting that this model is relatively new to the field. These mice will undoubtedly prove invaluable to future studies of steroid hormones in normal development and function. The ER alpha KO mouse has been and continues to be utilized to further study the role of estrogen action in the cardiovascular system. bone physiology, behavior, the immune system, neurophysiology, and adipogenesis. Furthermore, studies of the documented "non-genomic" effects of estradiol and progesterone in the brain as well as ligand-independent actions involving cross-talk with other signaling systems will be advanced with further investigations using the ER alpha KO mouse. And finally, the ER alpha KO in combination with the recently developed ER beta KO mouse will prove invaluable in distinguishing the different roles that may exist between the two receptors in the estrogen signaling system.

Animals↗
PubMed1996

Qualitative process modeling of cell-cell-pathogen interactions in the immune system.

We present a general cell behavior modelling system for immune functions, based on qualitative process theory. Model system heuristics integrate known characteristics and processes of cells, pathogens, antibodies, antigens, and cytokines. The system generates qualitative simulations of primary immune responses to bacterial and viral infections. Model heuristics can be mapped to a free-running cellular automata-like simulation that demonstrates quantitative behaviors of actor populations. This system serves as a tool for testing assumptions about cellular functions in immunity, as well the basis for a qualitative discovery system that may infer new process heuristics based on evaluation of experimental data.

Artificial Intelligence↗
PubMed1999

Polydnavirus-mediated suppression of insect immunity.

Polydnaviruses are symbiotic proviruses of some ichneumonid and braconid wasps that modify the physiology, growth and development of host lepidopteran larvae. Polydnavirus infection targets neuroendocrine and immune systems, altering behavior, stunting growth, and immobilizing immune responses to wasp eggs and larvae. Polydnavirus-mediated disruption of cellular and humoral immunity renders parasitized lepidopteran larvae suitable for development of wasp larvae as well as more susceptible to opportunistic infections. Evidence from the Campoletis sonorensis polydnavirus system indicates that the unique genomic organization of polydnaviruses may have evolved to amplify the synthesis of immunosuppressive viral proteins. Immunosuppressive viruses have been essential to elucidating vertebrate immunity. Polydnaviruses have similar potential to clarify insect immune responses and may also provide novel insights into the role of insect immunity in shaping polydnavirus genomes.

Journal Article↗
PubMed1996

Cytokines and food intake: the relevance of the immune system to the student of ingestive behavior.

The aims of this paper are to provide a selective review of the literature relating immune system mediators, especially cytokines, to the control of eating and to indicate why this literature is particularly relevant to the student of ingestive behavior. Four reasons are given. Firstly, many immune system mediators influence eating, providing excellent examples of neuroimmunological controls of behaviour. Secondly, the immune system appears to be involved in the profound eating pathology associated with several clinical conditions. Thirdly, cytokines affect both energy intake and energy expenditure. Fourthly, the anorexia typically associated with activation of the immune system provides an informative model for the analysis of gut-brain communication in the control of eating.

Body Weight↗
PubMed1987

Behavioral influences on the immune system: stress and conditioning.

Several investigators have demonstrated that immune responses may be subject to classical conditioning processes. Conditioning effects in both cell-mediated and humoral immune responses have been reported. Strong evidence for behavioral effects on immune responses has been provided by studies of stress-induced immunosuppression. Stressors may increase morbidity due to infectious agents, depress antibody responses, inhibit lymphocyte reactions, and attenuate several other cell-mediated immune functions. In our studies, acute inescapable footshock inhibited natural killer cell (NK) activity in CD-1 and C57BL/6J mice, but not in DBA/2J mice. Genetic factors play a role in the immunological responses to stress. In contrast to the effects of acute stress, NK activity of mice exposed to chronic inescapable footshock was not reduced from control levels. Adaptive processes may be invoked during repeated stress exposure, thereby limiting the potentially damaging effects of the stressor.

Animals↗
PubMed1994

Early postnatal diazepam treatment of rats and neuroimmunocompetence in adulthood and senescence.

Functional teratogenic risk of perinatal diazepam (D) treatment was studied in animal model experiments using early postnatal D administration in rats (single dose of 10 mg/kg sc in 7-day-old pups) and long-term follow-up till the age of 18 months with monitoring of behavior, reproductive functions, brain biochemical variables, and immune system reactivity. Behavioral tests carried out at the age of 6, 12, and 18 months indicated higher emotionality and deviations of novelty reaction in D rats in comparison with controls, and these differences decreased with aging. However, no deficits were found in memory testing. D rats revealed some transitional alterations of monoamine neurotransmission in the hypothalamus (5-HT) and striatum (DA) and minor defects in reproductive functions (irregular estrous cycles in females). Significant depression of immune response in D rats persisting for the whole life may be considered as a serious risk of neonatal D treatment.

Aging↗
PubMed2002

Modulating the modulators: parasites, neuromodulators and host behavioral change.

Neuromodulators can resculpt neural circuits, giving an animal the behavioral flexibility it needs to survive in a complex changing world. This ability, however, provides parasites with a potential mechanism for manipulating host behavior. This paper reviews three invertebrate host-parasite systems to examine whether parasites can change host behavior by secreting neuromodulators. The parasitic wasp, Cotesia congregata, suppresses host feeding partly by inducing the host (Manduca sexta) to increase the octopamine concentration in its hemolymph. The increased octopamine concentration disrupts the motor pattern produced by the frontal ganglion, preventing the ingestion of food. Polymorphus paradoxus (Acanthocephalan) alters the escape behavior of its host, Gammarus lacustris (Crustacea), possibly through an effect on the host's serotonergic system. The trematode Trichobilharzia ocellata inhibits egg-laying in its snail host (Lymnaea stagnalis), partly by inducing the host to secrete schistosomin. Schistosomin decreases electrical excitability of the caudodorsal cells. The parasite also alters gene expression for some neuromodulators within the host's central nervous system. In at least two of these three examples, it appears that the host, not the parasite, produces the neuromodulators that alter host behavior. Producing physiologically potent concentrations of neuromodulators may be energetically expensive for many parasites. Parasites may exploit indirect less energetically expensive methods of altering host behavior. For example, parasites may induce the host's immune system to produce the appropriate neuromodulators. In many parasites, the ability to manipulate host behavior may have evolved from adaptations designed to circumvent the host's immune system. Immune-neural-behavioral connections may be pre-adapted for parasitic manipulation.

Animals↗
PubMed2001

Nonlinear determinism in the immune system. In vivo influence of electromagnetic fields on different functions of murine lymphocyte subpopulations.

Animal studies of the effects of low-frequency electromagnetic fields (EMFs) on the immune system appear inconsistent, and recent evidence indicates that inconspicuous experimental problems are not responsible. We hypothesized that the inconsistencies resulted from use of linear methods and models to study inherently nonlinear input-output relationships. Using a novel analytical method, we found that exposure of mice to 5 G, 60 Hz, for 1-105 days in 6 independent experiments consistently affected a broad panel of immune variables when and only when the reaction of the immune system was modeled to allow the possibility of nonlinearity in the relationship between the field and the immune variables. It was possible to mimic the pattern observed in the immune data by sampling from a known chaotic system, suggesting the possibility that the observed pattern was the result of intrinsic nonlinear regulatory mechanisms in the immune system. Overall, the results suggested that lymphoid sub-populations were vulnerable to the physiological consequences of EMF transduction, that it may never be possible to predict specific changes in particular immune-system variables, and that the underlying behavior of the immune system (that which occurs in the absence of specific inputs) may be governed by laws that manifest extreme sensitivity to prior states.

Animals↗
PubMed2001

Immunoalienation. A behavioral analysis of the immune system.

Immunoalienation denotes the process through which the definition of self, as defined by the immune system, progressively deviates from the genetically determined definition of self. The mechanisms responsible for immunoalienation are discussed in light of the available evidence. The different kinds of immunoalienation are analyzed, and their theoretical as well as practical implications to disease, tumors, and transplant biology are briefly discussed.

Antigen-Antibody Reactions↗
PubMed1997

Intracerebroventricular porcine corticotropin-releasing hormone and cortisol effects on pig immune measures and behavior.

The effects of intracerebroventricular (icv) administration of porcine corticotropin-releasing hormone (pCRH) and cortisol on the immune system and behavior were examined in domestic pigs. In Experiment 1, 50 micrograms of pCRH in 200 microliters of saline or 200 microliters of vehicle was administered i.c.v. at 0600 h. Blood samples were obtained at 0600 (prior to injection), 0700, and 0800 h. Plasma cortisol concentrations were higher at 1 and 2 h after pCRH than after saline. Generally, pCRH failed to effect NK cytotoxicity or lymphocyte proliferation in response to phytohemagluttin (PHA). However, 1 h postinjection, pigs administered pCRH i.c.v. had marginally lower NK activity than control pigs. Pigs injected with pCRH had substantially lower neutrophil chemotaxis (CHTX) than the control pigs at 1 and 2 h postinjection. As blood cortisol concentration increased, neutrophil CHTX decreased. Pigs injected i.c.v. with pCRH had higher neutrophil numbers and neutrophil:lymphocyte ratios than control pigs. Percentage of lymphocytes was higher among control than treated pigs. Central pCRH increased overall activity, particularly walking, standing, licking, rooting, and increased activity-related sequences (e.g., sit, walk and stand, walk), but reduced complex oral/nasal sequences (e.g., root, lick). In Experiment 2, pigs were injected i.c.v. with 10 micrograms of cortisol in 200 microliters of saline or with vehicle at 0600 h. Administration of cortisol failed to effect NK cytotoxicity, lymphocyte proliferation, CHTX, or leukocyte distribution. Pigs given cortisol had no apparent change in behavior. These data indicate leukocyte distribution and specific neutrophil function in pigs were significantly modulated by stress-related hormones of the hypothalamic-pituitary-adrenal axis and complexity of behavioral sequences (pigs repeating certain behavioral sequences) associated with increased activity was reduced. Oral/nasal stereotypies (as seen among confined sows) were not elevated among pigs given i.c.v. pCRH. CRH given by i.c.v. administration may serve as a better model for acute rather than chronic stress.

Animals↗
PubMed2005

Neural and behavioral responses to systemic immunologic stimuli: a consideration of bacterial T cell superantigens.

Immune responses represent a source of systemic stress which impacts the brain and modifies various neuroendocrine and behavioral functions. Therefore, the immune system has been conceived of as a potential contributor to stress-related behavioral abnormalities, such as depression. Much of this knowledge has been gained through research focused largely on the administration of cytokines and/or bacterial endotoxin (eg., LPS), which targets innate immune cells, such as macrophages. However, fewer studies have addressed the effects of T cell activation on central nervous system (CNS) function. The discovery and characterization of bacterial superantigens (SAgs) has introduced an important opportunity for studying how T cell activation influences CNS function. Superantigens target unique variable regions of the beta chain of the mouse and human T cell receptor. This is restricted by the class II molecule of the major histocompatibility complex (MHC), and results in the production of a cytokine cascade that includes interleukin-2 (IL-2), interferon-gamma (IFNgamma), tumor necrosis factor (TNF) and many other cytokines, including IL-6. The best studied SAgs are the staphylococcal enterotoxins, of which staphylococcal enterotoxins A and B (SEA and SEB), have been shown to produce significant changes in behavior and activation of the hypothalamic-pituitary-adrenal (HPA) axis. Importantly, a T cell requirement was necessary to produce these changes. Furthermore, the anorexic or hypophagic effects of SAg challenge in mice appears to be related to anxiety-like processes, since challenge with both SEA or SEB reduces consumption of mainly novel food or food presented in a novel context. In the present paper, these studies are reviewed and related to known alterations in both anxiogenic and anxiolytic neuropeptides. It is suggested that immunologically-induced changes in the brain activate both categories of neuropeptides, thereby sustaining an adaptive state of arousal that promotes appropriate behavioral adjustments during infectious illness.

Animals↗
PubMed2000

Reduced interleukin-1 responsiveness in immune system and central nervous system of inbred polydipsic (STR/N) mice.

Inbred polydipsic mice (STR/N strain) have primary polydipsia. The previous studies found abnormalities in the central nervous system (CNS), especially in the hypothalamus and circumventricular organ. As a part of pursuing to find the cause of the polydipsia, we investigated immunological characteristics of STR/N mice, using the ICR strain of mice as control. Their thymic subset cells showed that CD4+CD8+ double positive cells were increased, CD4+ single positive cells were decreased and CD5 expression was deficient, compared to ICR mice. T cell proliferative response and interleukin (IL)-2 production caused by IL-1beta stimulation were reduced in STR/N mice than those in the ICR mice. In in vivo studies the degree of thymic atrophy and the increases in serum level of ACTH and corticosterone induced by intraperitoneal IL-1beta injection were much less in STR/N mice than those in controls. Furthermore, adipsic response also induced by IL-1beta injection was greatly reduced compared to their control mice. All these results suggest that the responsiveness to IL-1 is impaired both in the immune system and the CNS of STR/N mice.

Adrenocorticotropic Hormone↗
PubMed2001

Chronic treatment with the atypical antidepressant tianeptine attenuates sickness behavior induced by peripheral but not central lipopolysaccharide and interleukin-1beta in the rat.

RATIONALE: The hypothesis that proinflammatory cytokines play a causative role in the pathophysiology of depression has been recently tested by studying the effect of antidepressants on production of endogenous cytokines, and on sickness behavior induced by exogenous cytokines. In this last case, however, the effect of antidepressants has been only studied on the effect of peripherally administered cytokines. OBJECTIVES: The aim of the present study was to determine whether the antidepressant tianeptine can attenuate both peripheral and central cytokine actions. METHODS: Rats were injected IP with acute (10 mg/kg) or chronic (10 mg/kg, 2 times/day, 17 days) tianeptine. The effects of this treatment were assessed on the behavioral (social exploration, locomotion) and metabolic (food intake, body weight) alterations induced by peripheral or central administration of the cytokine inducer lipopolysaccharide (LPS) (250 microg/kg IP; 100 ng/rat ICV) or the prototypical proinflammatory cytokine interleukin-1 (IL-1)beta (15 microg/rat IP; 90 ng/rat ICV). RESULTS: Chronic, but not acute, treatment with tianeptine attenuated the behavioral signs of sickness behavior induced by peripheral, but not central, LPS or IL-1beta. CONCLUSIONS: This work, which is the first in vivo study assessing the effect of an antidepressant on centrally induced immune activation, shows a clear dissociation between peripheral and central cytokine effects, and suggests a peripheral site of action of tianeptine. It also provides the first evidence that the protective effects of classical antidepressants on LPS-induced sickness behavior extend to an atypical antidepressant, and that the protective effect of antidepressants also applies to IL-1beta.

Animals↗