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PubMed1990

Interactions between the brain and the immune system.

The observations and research described in this communication derive from a nontraditional view of the immune system. It has become abundantly clear that there are probably no organ systems or homeostatic defense mechanisms that are not, in vivo, subject to the influence of interactions between behavioral and physiological events. The complex mechanisms underlying these interactions and their relationship to health and illness, however, are imperfectly understood. The most imperfectly understood, perhaps, are the interrelationships among brain, behavior, and immune processes. Without attempting to cover all the literature, we have used stress effects and conditioning phenomena as illustrations to point out that behavior can influence immune function. We have also described data indicating that the immune system can receive and respond to neural and endocrine signals. Conversely, behavioral, neural, and endocrine responses seem to be influenced by an activated immune system. Thus, a traditional view of immune function that is confined to cellular interactions occurring within lymphoid tissues is insufficient to account for changes in immunity observed in subhuman animals and man under real world conditions. These data question seriously the notion of an autonomous immune system. Most of the research on the regulation of immune responses has been predicated on the assumption that such regulation is accomplished by the interacting components of the immune system itself, e.g. interactions among helper and suppressor T-lymphocytes, B-cells, and accessory cells that can result in the production of antibody and effector T cells. The immune system is, indeed, capable of considerable self-regulation, and immune responses can be made to take place in vitro. The functions of that component of adaptive processes known as the immune system that are of ultimate concern, however, are those that take place in vivo. There are now compelling reasons to believe that in vivo immunoregularity processes influence and are influenced by the neuroendocrine environment in which such processes actually take place--an environment that, on the one hand, can generate signals that resting and/or activated leukocytes can receive, and, on the other hand, is exquisitely sensitive to the individual's perception of and capacity to adapt to the demands of the environment. The immune system appears to be modulated, not only by feedback mechanisms mediated through neural and endocrine processes, but by feedforward mechanisms as well. The immunologic effects of learning, an essential feedforward mechanism, suggest that, like direct neural and endocrine processes, behavior can, under appropriate circumstances, serve an immunoregulatory function in vivo.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2005

Stimulation of cell component of the immune response activates exploratory behavior in senescence accelerated OXYS rats.

Suppression of the cell component of the immune system and open-field behavior developing in OXYS rats by the age of 3 months are regarded as manifestations of accelerated aging. Stimulation of cell-mediated immune response with BCG vaccine caused a dose-dependent increase of orientation and exploratory activity of OXYS rats in the open field test to virtually the same level as in Wistar rats.

Aging↗
PubMed1995

Rapid changes in cellular immunity following a confrontational role-play stressor.

Recent laboratory studies have shown several immune system changes consistently associated with brief stress including increases in circulating natural killer (NK) cell numbers, increases in NK cell cytotoxicity (NKCC), increases in suppressor cytotoxic (CD8) T cell numbers, and decreases in the in vitro proliferative response to mitogen stimulation. In the present study, we use a confrontational role-play, which brings out responses varying from assertion to capitulation and examine the psychological, behavioral, physiological, and immune system responses to this task compared to a resting control task. Compared to the control condition, the brief confrontational role-play led to significant subjective and physiological arousal and increases in circulating NK (CD16, CD56) as well as large granular lymphocyte (CD57) cells and suppressor/cytotoxic T cells (CD8). There were also significant relationships between stress-related increases in the cardiovascular measures and the numbers of circulating NK cells. These findings support sympathetic nervous system activation as a primary mechanism for increases in NK cell numbers under challenge. These role-play results are generally consistent with those from other laboratory tasks such as mental arithmetic. However, in contrast to previously examined brief stressors, the role-play led to decreased NKCC adjusted for percentage of NK cells. This apparent differential change in NK cytotoxicity across different types of activating experimental tasks points to the importance of examining dimensions of the behavioral and emotional response to challenge or threat in addition to that of autonomic arousal.

Adult↗
PubMed2006

Comparative psychoneuroimmunology: evidence from the insects.

Interactions between immune systems, nervous systems, and behavior are well established in vertebrates. A comparative examination of these interactions in other animals will help us understand their evolution and present adaptive functions. Insects show immune-behavioral interactions similar to those seen in vertebrates, suggesting that many of them may have a highly conserved function. Activation of an immune response in insects results in illness-induced anorexia, behavioral fever, changes in reproductive behavior, and decreased learning ability in a broad range of species. Flight-or-fight behaviors result in a decline in disease resistance. In insects, illness-induced anorexia may enhance immunity. Stress-induced immunosuppression is probably due to physiological conflicts between the immune response and those of other physiological processes. Because insects occupy a wide range of ecological niches, they will be useful in examining how some immune-behavioral interactions are sculpted by an animal's behavioral ecology.

Animals↗
PubMed2003

Parameters of cell immune response in Wistar and OXYS rats and their behavior in the open field test.

Comparative analysis of the state of the thymus, activity of cell component of the immune system, and open field behavior of Wistar and OXYS rats showed early involution of the thymus in OXYS rats. By morphological picture this involution corresponded to accidental involution and was paralleled by low level of delayed hypersensitivity reaction and by inhibition of motor and exploratory behavior.

Animals↗
PubMedDate not supplied

Cytokine-neurotransmitter interactions in the brain.

The data reviewed in this study show that immune-active molecules, such as infectious agents and their components, and cytokines, may induce profound alterations in several neurotransmitters in the CNS. The activation of the immune system elicits fever, behavioral and neuroendocrine changes and may be involved in neuropathological changes occurring in CNS conditions. These effects may be achieved through and accounted for by the changes induced in central neurotransmitters and in the neuroendocrine system by immune challenges. The present review will summarize the available evidence of the reciprocal interactions between cytokines and neurotransmitters in the CNS.

Animals↗
PubMed1998

Cytokine-neurotransmitter interactions in the brain

The data reviewed in this study show that immune-active molecules, such as infectious agents and their components, and cytokines, may induce profound alterations in several neurotransmitters in the CNS. The activation of the immune system elicits fever, behavioral and neuroendocrine changes and may be involved in neuropathological changes occurring in CNS conditions. These effects may be achieved through and accounted for by the changes induced in central neurotransmitters and in the neuroendocrine system by immune challenges. The present review will summarize the available evidence of the reciprocal interactions between cytokines and neurotransmitters in the CNS.

Journal Article↗
PubMed2006

Immunity and behavior: antibodies alter emotion.

Systemic lupus erythematosus is an autoimmune disease in which most patients express Abs that bind double-stranded DNA. Recent work has shown that a subset of lupus Abs can crossreact with the NR2A and NR2B subunits of the NMDA receptor. This receptor is expressed in neurons throughout the brain but is at highest density within cells of the hippocampus, amygdala, and hypothalamus. The neurons in the CNS are normally protected from brain-reactive Abs by the blood-brain barrier (BBB); however, a breach in the barrier's integrity exposes neurons to potentially pathogenic Abs. Previously, we have shown that mice that are immunized with a peptide mimetope of DNA produce lupus-like Abs that crossreact with DNA and the NMDA receptor. Moreover, after abrogation of the BBB by treatment with lipopolysaccharide, the immunized mice display hippocampal neuron damage with ensuing memory impairment. Given that rises in epinephrine can increase cerebral blood flow and can cause leaks in the BBB, we decided to investigate whether epinephrine could act as a permissive agent for Ab-mediated neurotoxicity. Here, we show that peptide-immunized mice, given epinephrine to open the BBB, lose neurons in the lateral amygdala and develop a behavioral disorder characterized by a deficient response to fear-conditioning paradigms. Thus, the agent used to open the BBB determines which brain region is made vulnerable to neurotoxic Abs, and Abs that penetrate brain tissue can cause changes not only in cognitive competence, but also in emotional behavior.

Amygdala↗
PubMed1988

Immune system. Relationship to anxiety disorders.

The demonstration that behavioral states and CNS processes are associated with immune function suggests that there may be a relationship between anxiety and the immune system. Stress and immunity have been studied extensively, but there have been relatively few studies of anxiety and immunity. Many of the neurobiologic processes associated with stress and with depression have been observed in anxiety and are known to influence the immune system. A review of the immune response to stress and of immune alterations in depression has been presented in an effort to provide further understanding of the biology of anxiety. It appears that a variety of factors such as age; sex; nature, intensity, and chronicity of a stressful life events; and psychologic response to life stress need to be considered in the investigation of behavior and immunity. The biologic effects of stress on immunity are multifaceted, including complex neuroendocrine and neurotransmitter interactions. Further investigation is required of anxiety and immunity in clearly delineated and diagnosed anxiety states and disorders. Such studies may help to elucidate the pathophysiology of anxiety disorders.

Anxiety Disorders↗
PubMed2004

Decrease of immobility behavior in forced-swimming test and immune system enhancing effect of traditional medicine Gamisipjundaebo-tang.

Gamisipjundaebo-tang (GSDBT) has been used for the purpose of development of physical strength. In the present study, we investigated the immune enhancing effect induced by GSDBT. We investigated the anti-immobility effect of GSDBT via a forced-swimming test and blood biochemical parameters related to fatigue, glucose, blood urea nitrogen, lactic dehydrogenase, creatine kinase, and total protein. GSDBT (0.1 and 1 g/kg) was orally administered to mice for 14 days. After 7 and 14 days, as assessed through a forced-swimming test, immobility time was decreased in the GSDBT-administrated group (0.1 and 1 g/kg) in comparison with the control group. In addition, after 8 days, the contents of glucose and lactate dehydrogenase in the blood serum were increased, and contents of blood urea nitrogen were decreased in the GSDBT-administrated group. After 15 days, the contents of glucose were increased, and the contents of lactate dehydrogenase and blood urea nitrogen were decreased in the GSDBT-administrated group. However, it had no effect on the elevation of creatine kinase and total protein level. We also investigated the effect of GSDBT on the production of cytokines in human T-cell line, MOLT-4 cells, and splenocytes. GSDBT significantly increased interferon (IFN)-gamma and interleukin (IL)-2 levels compared with the media control but did not affect IL-4. GSDBT increased the protein expression of IFN-gamma in MOLT-4 cells. These results suggest that GSDBT may be useful in immune function improvement and may also have antifatigue properties.

Animals↗
PubMed2000

A mathematical method for investigating dynamic behavior of an idiotype network of the immune system. The time minimum optimal control theory.

We proposed a mathematical method to investigate an integrated property of an idiotype immune network under the time minimum optimal control. The transient changes of amounts of B cell receptor bound antibodies and immune complex in the network system were expressed by detailed differential equations. The rate constant for binding the second Fab arm of antibody was set as a function of coulombic repulsive force to express the influence of redistribution of electrical charges in the ligand-receptor molecular complex. We proposed time minimum optimal control strategy as an organizing principle for rapid reactions of the immune system. Based on the rigorous mathematical foundations of the optimal control theory, we determined the differential equations for co-state variables for the state variables to compute the time minimum transient changes in the amount of the species. Biological parameters in the immune reactions were utilized from the reported experimental data. Numerical computation disclosed that influence of changes in a rate constant extended to all the species of the network. Changes in a rate constant in a different B cell system reinforced the collaborations among the idiotypes and lead them to set in motion the ejection of the antigen. Simulation of reported experimental data by the present method was successful. There were, however, some inevitable dissociations between reported experimental data and computed results. The present method will be available for evaluating the time minimum reaction of the immune network system.

Journal Article↗
PubMed1996

Stress and the immune system in the etiology of anxiety and depression.

There is clinical and experimental evidence that various aspects of the immune and endocrine systems are severely compromised in chronic stress and depression. For example, it has been shown that a reduced lymphocyte response occurs to mitogens in depressed patients, effects that are not reversed by chronic antidepressant treatment. By contrast, monocyte phagocytosis is increased, while neutrophil phagocytosis is decreased in depressed patients. Such changes are normalized by effective antidepressant treatment. The results of such studies and others that demonstrate alterations in noncellular immune processed in depression indicate that the changes in immune function correlate with the severity and duration of the external and/or internal stressful stimuli. There is evidence that some of the immune changes are a reflection of increased plasma glucocorticoids that characterize both stress and depression. However, it is also apparent that the cytokines, prostaglandins, and corticotrophic releasing factor (CRF) also play an important role in initiating the behavioral and pathophysiological changes that are characteristic of both depression and chronic stress. This review attempts to critically assess the interplay between CRF, the immune and neurotransmitter systems, and behavior in chronic stress and depression.

Animals↗
PubMed2004

Elaborate interactions between the immune and nervous systems.

The immune system and the nervous system maintain extensive communication, including 'hardwiring' of sympathetic and parasympathetic nerves to lymphoid organs. Neurotransmitters such as acetylcholine, norepinephrine, vasoactive intestinal peptide, substance P and histamine modulate immune activity. Neuroendocrine hormones such as corticotropin-releasing factor, leptin and alpha-melanocyte stimulating hormone regulate cytokine balance. The immune system modulates brain activity, including body temperature, sleep and feeding behavior. Molecules such as the major histocompatibility complex not only direct T cells to immunogenic molecules held in its cleft but also modulate development of neuronal connections. Neurobiologists and immunologists are exploring common ideas like the synapse to understand properties such as memory that are shared in these two systems.

Animals↗
PubMed1998

Environmental endocrine modulators and human health: an assessment of the biological evidence.

Recently, a great deal of attention and interest has been directed toward the hypothesis that exposure, particularly in utero exposure, to certain environmental chemicals might be capable of causing a spectrum of adverse effects as a result of endocrine modulation. In particular, the hypothesis has focused on the idea that certain organochlorine and other compounds acting as weak estrogens have the capability, either alone or in combination, to produce a variety of adverse effects, including breast, testicular and prostate cancer, adverse effects on male reproductive tract, endometriosis, fertility problems, alterations of sexual behavior, learning disability or delay, and adverse effects on immune and thyroid function. While hormones are potent modulators of biochemical and physiological function, the implication that exposure to environmental hormones (e.g., xenoestrogens) has this capability is uncertain. While it is reasonable to hypothesize that exposure to estrogen-like compounds, whatever their source, could adversely affect human health, biological plausibility alone is an insufficient basis for concluding that environmental endocrine modulators have adversely affected humans. Diethylstilbestrol (DES) is a potent, synthetic estrogen administered under a variety of dosing protocols to millions of women in the belief (now known to be mistaken) that it would prevent miscarriage. As a result of this use, substantial in utero exposure to large numbers of male and female offspring occurred. Numerous studies have been conducted on the health consequences of in utero DES exposure among the adult offspring of these women. There are also extensive animal data on the effects of DES and there is a high degree of concordance between effects observed in animals and humans. The extensive human data in DES-exposed cohorts provide a useful basis for assessing the biological plausibility that potential adverse effects might occur following in utero exposure to compounds identified as environmental estrogens. The effects observed in both animals and humans following in utero exposure to sufficient doses of DES are consistent with basic principles of dose response as well as the possibility of maternal dose levels below which potential non-cancer effects may not occur. Significant differences in estrogenic potency between DES and chemicals identified to date as environmental estrogens, as well as an even larger number of naturally occurring dietary phytoestrogens, must be taken into account when inferring potential effects from in utero exposure to any of these substances. The antiestrogenic properties of many of these same exogenous compounds might also diminish net estrogenic effects. Based on the extensive data on DES-exposed cohorts, it appears unlikely that in utero exposure to usual levels of environmental estrogenic substances, from whatever source, would be sufficient to produce many of the effects (i.e., endometriosis, adverse effects on the male reproductive tract, male and female fertility problems, alterations of sexual behavior, learning problems, immune system effects or thyroid effects) hypothesized as potentially resulting from exposure to chemicals identified to date as environmental estrogens.

Adult↗
PubMed2006

Lipopolysaccharide has indomethacin-sensitive actions on Fos expression in topographically organized subpopulations of serotonergic neurons.

Peripheral immune activation results in physiological and behavioral responses including changes in the level of behavioral arousal. One mechanism through which immune activation can influence these responses is via actions on brainstem neuromodulatory systems, including serotonergic systems. To investigate the effects of peripheral immune activation on serotonergic systems and behavior, and the potential role of prostanoids in mediating these effects, we compared the effects of intraperitoneal injections of lipopolysaccharide (LPS), in the presence or absence of the cyclooxygenase inhibitor indomethacin, on total plasma L-tryptophan concentrations, Fos expression in subdivisions of the brainstem raphe complex, and home cage behaviors. Peripheral LPS administration had no effect on total plasma L-tryptophan concentrations but increased Fos expression in serotonergic neurons selectively within the interfascicular (DRI) and ventrolateral (DRVL) subdivisions of the dorsal raphe nucleus 4 h following treatment; pretreatment with indomethacin blocked the LPS-induced increases in Fos expression within the DRI and DRVL. Peripheral LPS administration decreased measures of behavioral arousal including locomotion, rearing, climbing, and self-grooming; LPS administration had no effect on these behaviors in mice pretreated with indomethacin. The indomethacin-sensitive effects of LPS on Fos expression in the DRI may be due to selective activation of Type II serotonergic neurons which are largely restricted to the DRI region and have unique afferent regulatory mechanisms and behavioral correlates. Further studies of the effects of peripheral immune activation on DRI serotonergic systems may lead to a better understanding of the relationships among immune function, serotonergic systems, and behavior.

Analysis of Variance↗
PubMed2005

Cytokines and sleep.

Personal experience and empirical data indicate sleep is altered during sickness. Important signaling molecules of the peripheral immune system called cytokines orchestrate responses to infection. Through a variety of mechanisms, the brain detects activation of the peripheral immune system. The brain responds to infection by altering physiological processes and complex behavior, including sleep. These changes in physiology and behavior collectively function to support the immune system, and under normal circumstances the health of the host is restored. Several of these cytokines, and their receptors, are present in normal healthy brain. Some cytokines regulate sleep under physiological conditions, in the absence of infection or immune challenge. For example, interleukin-1 directly alters discharge patterns of neurons in hypothalamic and brainstem circuits implicated in the regulation of sleep-wake behavior. Many other cytokines modulate sleep because they interact with neurotransmitter, peptide, and/or hormone systems to initiate a cascade of responses that subsequently alter sleep-wake behavior. Because cytokines regulate/modulate sleep-wake behavior in the absence of immune challenge, and cytokine concentrations and profiles are altered during infection, it is likely that cytokines mediate infection-induced alterations in sleep. Whether the changes in sleep that occur during infection are beneficial and aid in recovery remains to be determined.

Bacterial Infections↗