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PubMed1985

[Clinical and experimental study of the host defense mechanism from the aspect of tumor immunology].

The host defense mechanism was fundamentally and clinically investigated from the aspect of tumor immunology. The behavior of macrophages in the immune systems of experimental animals demonstrated different patterns of response in the bone marrow, peritoneal cavity and spleen, respectively. It was doubtless that the spleen occasionally exerted an immunosuppressive action. Ectopic immunization of syngeneic rats with normal liver cells resulted in specific inhibition of the growth of the tumor cells (AH-I30) derived from liver. This seemed to strongly suggest a local immune response. In clinical cases, the host defense mechanism was found to collapse due to surgical intervention, malnutrition and immunosuppressive substances. The relation between complements and host defense mechanism has been controversial. Our studies indicated the serum complement level to be the most reliable parameter for understanding the host defense mechanism. Since the combination of immunostimulants and anticancer drugs is likely to induce anticancer drugs to exert an adverse effect depending on the time of such combination, timing of combined administration of drugs should be chosen with great care.

Animals↗
PubMedDate not supplied

Neglected factors in cancer treatment: cellular interactions and dynamic microenvironment in solid tumors.

Solid tumors are "organoids" consisting of highly heterogeneous populations of malignant, stromal and inflammatory cells and dynamic extracellular matrix. In particular, distinct cellular microenvironments are observed. The survival strategies of malignant cells might therefore be highly differentiated, causing the high genotypic and phenotypic instability characteristic of malignant cells in vivo. A constant interplay between the tumor compartments and the host immune and hemostatic systems determines the behavior of the tumor. A description of typical microenvironments and of cellular and matrix interactions is provided. Based on these, it is here postulated that: (a) any cancer treatment, by influencing differently the various tumor compartments, will alter previously established equilibria; (b) the behavior (growth, invasiveness, metastatic potential, resistance to further treatment) of a malignancy after treatment might be altered with respect to what is assumed in terms of effect of the treatment on the malignant cells alone.

Cell Communication↗
PubMed1998

Open-field and LPS-induced sickness behavior in young chickens: effects of embryonic cocaine and/or ritanserin.

Exposure to drugs of abuse during embryogenesis may adversely affect nervous, immune, and endocrine systems development. We compared exposure on embryonic day 18 (E18) by single or multiple cocaine (COC) injections (56.25 mg/kg total dose for both) or saline on hatching and activity measures. In saline-exposed controls, repeated testing, age, and gender affected activity levels. A single or multiple COC injections increased the median latency to explore and multiple COC injections decreased the median number of lines crossed by female chicks in the open field. We also determined if pretreatment with the serotonin2 (5-HT2) receptor antagonist ritanserin could attenuate COC's effects on open-field behavior as well as behaviors sensitive to immune system stimulation (lipopolysaccharide (LPS)-induced sickness behavior). Eggs containing embryos were pretreated on E17 with 0.4 mg ritanserin/kg or its vehicle followed by multiple COC injections or saline on E18. E18 COC treatment decreased the median number of lines crossed and distress vocalizations in females. Ritanserin pretreatment mitigated the COC induced effects. E18 COC exposure also suppressed LPS-induced sickness behaviors in both males and females, increasing food consumption and the time spent awake and active, as well as decreasing the time spent sleeping. Ritanserin alone had no effect on the food consumed or time spent active, nor did this dose affect COC-induced alterations in sickness behavior. Ritanserin alone decreased time spent sleeping and also failed to affect the COC-induced suppression. Thus, embryonic COC exposure can suppress open field and LPS-induced sickness behavior in the young chick, and ritanserin pretreatment can block the former, but not the latter effects at the dose chosen for these experiments.

Animals↗
PubMed2006

Pineal-dependent and -independent effects of photoperiod on immune function in Siberian hamsters (Phodopus sungorus).

Siberian hamsters (Phodopus sungorus) exhibit reproductive and immunological responses to photoperiod. Short (<10-h light/day) days induce gonadal atrophy, increase leukocyte concentrations, and attenuate thermoregulatory and behavioral responses to infection. Whereas hamster reproductive responses to photoperiod are dependent on pineal melatonin secretion, the role of the pineal in short-day induced changes in immune function is not fully understood. To examine this, adult hamsters were pinealectomized (PINx) or sham-PINx, and transferred to short days (9-h light/day; SD) or kept in their natal long-day (15-h light/day; LD) photoperiod. Intact and PINx hamsters housed in LD maintained large testes over the next 12 weeks; sham-PINx hamsters exhibited gonadal regression in SD, and PINx abolished this effect. Among pineal-intact hamsters, blood samples revealed increases in leukocyte, lymphocyte, CD62L+ lymphocyte, and T cell counts in SD relative to LD; PINx did not affect leukocyte numbers in LD hamsters, but abolished the SD increase in these measures. Hamsters were then treated with bacterial lipopolysaccharide (LPS), which induced thermoregulatory (fever), behavioral (anorexia, reductions in nest building), and somatic (weight loss) sickness responses in all groups. Among pineal-intact hamsters, febrile and behavioral responses to LPS were attenuated in SD relative to LD. PINx did not affect sickness responses to LPS in LD hamsters, but abolished the ameliorating effects of SD on behavioral responses to LPS. Surprisingly, PINx failed to abolish the effect of SD on fever. In common with the reproductive system, PINx induces the LD phenotype in most aspects of the immune system. The pineal gland is required for photoperiodic regulation of circulating leukocytes and neural-immune interactions that mediate select aspects of sickness behaviors.

Animals↗
PubMed2002

Hypothalamic-pituitary-adrenal axis, neuroendocrine factors and stress.

The stress system coordinates the adaptive responses of the organism to stressors of any kind.(1). The main components of the stress system are the corticotropin-releasing hormone (CRH) and locus ceruleus-norepinephrine (LC/NE)-autonomic systems and their peripheral effectors, the pituitary-adrenal axis, and the limbs of the autonomic system. Activation of the stress system leads to behavioral and peripheral changes that improve the ability of the organism to adjust homeostasis and increase its chances for survival. The CRH and LC/NE systems stimulate arousal and attention, as well as the mesocorticolimbic dopaminergic system, which is involved in anticipatory and reward phenomena, and the hypothalamic beta-endorphin system, which suppresses pain sensation and, hence, increases analgesia. CRH inhibits appetite and activates thermogenesis via the catecholaminergic system. Also, reciprocal interactions exist between the amygdala and the hippocampus and the stress system, which stimulates these elements and is regulated by them. CRH plays an important role in inhibiting GnRH secretion during stress, while, via somatostatin, it also inhibits GH, TRH and TSH secretion, suppressing, thus, the reproductive, growth and thyroid functions. Interestingly, all three of these functions receive and depend on positive catecholaminergic input. The end-hormones of the hypothalamic-pituitary-adrenal (HPA) axis, glucocorticoids, on the other hand, have multiple roles. They simultaneously inhibit the CRH, LC/NE and beta-endorphin systems and stimulate the mesocorticolimbic dopaminergic system and the CRH peptidergic central nucleus of the amygdala. In addition, they directly inhibit pituitary gonadotropin, GH and TSH secretion, render the target tissues of sex steroids and growth factors resistant to these substances and suppress the 5' deiodinase, which converts the relatively inactive tetraiodothyronine (T(4)) to triiodothyronine (T(3)), contributing further to the suppression of reproductive, growth and thyroid functions. They also have direct as well as insulin-mediated effects on adipose tissue, ultimately promoting visceral adiposity, insulin resistance, dyslipidemia and hypertension (metabolic syndrome X) and direct effects on the bone, causing "low turnover" osteoporosis. Central CRH, via glucocorticoids and catecholamines, inhibits the inflammatory reaction, while directly secreted by peripheral nerves CRH stimulates local inflammation (immune CRH). CRH antagonists may be useful in human pathologic states, such as melancholic depression and chronic anxiety, associated with chronic hyperactivity of the stress system, along with predictable behavioral, neuroendocrine, metabolic and immune changes, based on the interrelations outlined above. Conversely, potentiators of CRH secretion/action may be useful to treat atypical depression, postpartum depression and the fibromyalgia/chronic fatigue syndromes, all characterized by low HPA axis and LC/NE activity, fatigue, depressive symptomatology, hyperalgesia and increased immune/inflammatory responses to stimuli.

Autonomic Nervous System↗
PubMed1985

Does the immune system communicate with the central nervous system? Interferon modifies central nervous activity.

The present investigation determined whether an immunomodulator agent modified the central nervous system activity as measured behaviorally and neurophysiologically. Two types of interferons (IFNs), alpha (alpha) and gamma (gamma), were applied locally (microiontophoretically) into various regions of the rat brain simultaneously with single neuron recording from the cerebral cortex, hippocampus, thalamus and hypothalamus. Of the various IFNs, only alpha-IFN altered single cell activity in all brain structures in a dose-dependent manner. Moreover, systemic administration of alpha-IFN altered the naloxone-induced abstinence syndrome in morphine-dependent rats. These observations suggest that immunomodulators such as alpha-IFN are capable of influencing directly central nervous system function as well as the immune system.

Animals↗
PubMed1994

Brain monoaminergic, neuroendocrine, and immune responses to an immune challenge in relation to brain and behavioral lateralization.

Host responses to immune challenges involve central neurotransmission, the hypothalamo-pituitary adrenal axis, and the immune system. In the present work, we investigated the possibility of an asymmetry in the modification of brain monoamine metabolism induced by a systemic injection of lipopolysaccharide (LPS) in adult female mice. We also studied the possible influence of behavioral lateralization, as assessed by a paw preference test, on the reactivity of the nervous, neuroendocrine, and immune systems to a LPS challenge. The results showed that LPS administration induced an enhanced brain activity as demonstrated by an increase in noradrenergic, serotoninergic, and dopaminergic metabolism. Increased serotonin metabolism, observed in the hypothalamus and hippocampus, only occurred on the left side. Furthermore, the increase in serotonin turnover in the medial hypothalamus, the elevation of plasma adrenocorticotropin levels, and the decrease in T lymphocyte proliferation were observed in right-handed and ambidextrous mice but not in left-handed animals. Taken together, the results demonstrate that an immune challenge could induce neurochemical, neuroendocrine, and immune responses similar to those of stress, suggesting that LPS may be a stress inducer. Interestingly, these responses that may be asymmetrically expressed appear to depend on behavioral lateralization.

Adrenocorticotropic Hormone↗
PubMed2002

Brain-immune interactions in sleep.

This chapter discusses various levels of interactions between the brain and the immune system in sleep. Sleep-wake behavior and the architecture of sleep are influenced by microbial products and cytokines. On the other hand, sleep processes, and perhaps also specific sleep states, appear to promote the production and/or release of certain cytokines. The effects of immune factors such as endotoxin and cytokines on sleep reveal species specificity and usually strong dependence on parameters such as substance concentration, time relative to administration or infection with microbial products, and phase relation to sleep and/or the light-dark cycle. For instance, endotoxin increased SWS and EEG SWA in humans only at very low concentrations, whereas higher concentrations increased sleep stage 2 only, but not SWS. In animals, increases in NREM sleep and SWA were more consistent over a wide range of endotoxin doses. Also, administration of pro-inflammatory cytokines such as IL-6 and IFN-alpha in humans acutely disturbed sleep while in rats such cytokines enhanced SWS and sleep. Overall, the findings in humans indicate that strong nonspecific immune responses are acutely linked to an arousing effect. Although subjects feel subjectively tired, their sleep flattens. However, some observations indicate a delayed enhancing effect on sleep which could be related to the induction of secondary, perhaps T-cell-related factors. This would also fit with results in animals in which the T-cell-derived cytokine IL-2 enhanced sleep while cytokines with immunosuppressive functions like IL-4 and L-10 suppressed sleep. The most straightforward similarity in the cascade of events inducing sleep in both animals and humans is the enhancing effect of GHRH on SWS, and possibly the involvement of the pro-inflammatory cytokine systems of IL-1 beta and TNF-alpha. The precise mechanisms through which administered cytokines influence the central nervous system sleep processes are still unclear, although extensive research has identified the involvement of various molecular intermediates, neuropeptides, and neurotransmitters (cp. Fig. 5, Section III.B). Cytokines are not only released and found in peripheral blood mononuclear cells, but also in peripheral nerves and the brain (e.g., Hansen and Krueger, 1997; März et al., 1998). Cytokines are thereby able to influence the central nervous system sleep processes through different routes. In addition, neuronal and glial sources have been reported for various cytokines as well as for their soluble receptors (e.g., Kubota et al., 2001a). Links between the immune and endocrine systems represent a further important route through which cytokines influence sleep and, vice versa, sleep-associated processes, including variations in neurotransmitter and neuronal activity may influence cytokine levels. The ability of sleep to enhance the release and/or production of certain cytokines was also discussed. Most consistent results were found for IL-2, which may indicate a sleep-associated increase in activity of the specific immune system. Furthermore, in humans the primary response to antigens following viral challenge is enhanced by sleep. In animals results are less consistent and have focused on the secondary response. The sleep-associated modulation in cytokine levels may be mediated by endocrine parameters. Patterns of endocrine activity during sleep are probably essential for the enhancement of IL-2 and T-cell diurnal functions seen in humans: Whereas prolactin and GH release stimulate Th1-derived cytokines such as IL-2, cortisol which is decreased during the beginning of nocturnal sleep inhibits Th1-derived cytokines. The immunological function of neurotrophins, in particular NGF and BDNF, has received great interest. Effects of sleep and sleep deprivation on this cytokine family are particularly relevant in view of the effects these endogenous neurotrophins can have not only on specific immune functions and the development of immunological memories, but also on synaptic reorganization and neuronal memory formation.

Animals↗
PubMed1998

A genetic basis for neuroendocrine-immune interactions.

Psychoneuroimmunology is an exciting, complex field that elucidates interactions among the nervous, endocrine, and immune systems. The contribution of psychosocial factors and behavioral processes to these interactions has been the focus of numerous studies designed to investigate the intricate pathways that are involved in the "mind-body connection." In addition, the effects of this connection on the development and progression of various disease conditions are of considerable interest. Although efforts have been made to identify the cellular and molecular mechanisms underlying these relationships, the impact of genetic makeup on the communication among these systems has yet to be fully realized. The development of sophisticated genetic analytical methods and gene mapping techniques now provide the "tools" to determine the influence of genetics on behavior-neuroendocrine-immune interactions--an area of study that may represent the next frontier in psychoneuroimmunology.

Genes↗
PubMed1994

Current challenges and future expectations in exercise immunology: back to the future.

The immune system response to exercise is multifaceted, depending on the nature of exercise. The motivation behind recent research on the immune response to exercise comes from four basic directions: (i) keeping competitive athletes healthy, based on the perception that athletes are susceptible to infectious illness during intense training and competition; (ii) community interest in health promotion, based on the beneficial effect of exercise in lessening the risk of other lifestyle-associated diseases such as heart disease; (iii) use of exercise as adjunct therapy to improve patient functional capacity in certain diseases such as acquired immune deficiency syndrome (AIDS) and cancer; and (iv) work in the field of psychoneuroimmunology showing significant interaction between the neuroendocrine and immune systems, and the role of lifestyle factors in modulating immune function. Future work in exercise immunology will focus on topics such as: identifying the role of neuroendocrine factors in regulating the immune response to exercise; understanding the effects and appropriate type of moderate exercise in patients with diseases which involve the immune system; and possible long-term role of regular exercise in preventing diseases such as cancer, or the decline in immune function which accompanies the aging process.

Aging↗
PubMed2003

The physiology of marriage: pathways to health.

Marriage is the central relationship for most adults and has beneficial effects for health. At the same time, troubled marriages have negative health consequences. This review outlines the physiological pathways through which marital relationships influence health based on a stress/social support model. In addition, we review recent findings suggesting that unhappy marriages are associated with morbidity and mortality. We then turn to studies of marital interaction that include assessment of physiological pathways through which marital functioning influences health: the cardiovascular, endocrine, and immune systems. Across these studies, negative and hostile behaviors during marital conflict discussions are related to elevations in cardiovascular activity, alterations in hormones related to stress, and dysregulation of immune function. Using recent conceptualizations of the physiological impact of chronic stress, we illustrate how physiological changes associated with marital functioning in these studies have long-term implications for health outcomes. Finally, we discuss future implications of current research for understanding the relationships among marital functioning, physiology, and health.

Adult↗
PubMed2006

Heat and social rank impact behavior and physiology of PRRS-virus-infected pigs.

Changes in thermal environment can invoke a stress response in pigs, which in turn can potentially impact their immune system and disease susceptibility. We investigated effects of heat stress and social rank on behavior, immune responsiveness, and performance of pigs challenged with porcine reproductive and respiratory syndrome (PRRS) virus. Sixty-four 7-week-old PRRS-naïve pigs were assigned to each of four experimental treatments consisting of a 2 x 2 factorial design: PRRS (PRRS- or PRRS+) and environmental temperature (24 degrees C or 32 degrees C). Blood samples were taken prior to and at days 7 and 14 post-inoculation, and alveolar macrophages were collected via bronchoalveolar lavage at day 14. Total white blood cell counts, natural killer cytotoxicity, macrophage numbers, macrophage subpopulations, and performance measures were all significantly affected by social rank, heat stress, and/or infection status of the pig. Heat stress and PRRS status also significantly influenced the amount of time pigs spent lying with or without contacting another animal. Cortisol and various immune measures were also affected by PRRS status. These results show not only that intranasal inoculation with PRRS virus affects physiological, behavioral, and performance measures in growing pigs, but that social rank influences pigs' immune responsiveness to PRRS as well. Moreover, heat stress does not have additive negative impact on physiological or performance traits in pigs challenged with PRRS virus.

Animals↗
PubMed2006

Evaluation of pegylated lipid nanocapsules versus complement system activation and macrophage uptake.

This work consisted in defining the in vitro behavior of pegylated lipid nanocapsules (LNC) toward the immune system. LNC were composed of an oily core surrounded by a shell of lecithin and polyethylene glycol (PEG) known to decrease the recognition of nanoparticles by the immune system. The "stealth" properties were evaluated by measuring complement activation (CH50 technique and crossed-immunoelectrophoresis (C3 cleavage)) and macrophage uptake. These experiments were performed on 20-, 50-, and 100-nm LNC before and after dialysis. A high density of PEG at the surface led to very low complement activation by LNC with a slight effect of size. This size effect, associated to a dialysis effect in macrophage uptake, was due to differences in density and flexibility of PEG chains related to LNC curvature radius. Thanks to a high density, 660-Da PEG provided LNC a steric stabilization and a protective effect versus complement protein opsonization, but this protection decreased with the increase of LNC size, especially versus macrophage uptake.

Animals↗
PubMed1991

Psychoneuroimmunology. Implications for oncology?

Accumulating evidence indicates that the central nervous system (CNS) may regulate the activity of the immune system. Although the overall significance of the immune system in cancer remains controversial, psychosocial influences on immune function could potentially provide a mechanism to account for some of the reports of an association between psychosocial factors and cancer prognosis.

Antibody Formation↗
PubMed1998

Behaviorally conditioned immunosuppression using cyclosporine A: central nervous system reduces IL-2 production via splenic innervation.

Bi-directional interactions between the central nervous system (CNS) and immune system are demonstrated by the modification of immune function using behavioral conditioning. However, the mechanisms by which the CNS achieves conditioned immunomodulation are still in question. Here, we report that the immunosuppressive effects of cyclosporine A (CsA) can be behaviorally conditioned in rats using saccharin as a gustatory conditioned stimulus. The conditioned effects were compared to control groups that received CsA paired with water (sham-conditioned), CsA injection on test days (CsA-treated), and unhandled rats (untreated). In conditioned animals, the mitogen-induced lymphocyte proliferation in the spleen is significantly suppressed, and the survival time of heterotopic heart allografts prolonged. These effects are paralleled by conditioned inhibition of IL-2 and IFN-gamma synthesis by splenocytes. Furthermore, the CNS-induced immunosuppression is mediated neuronally and not via the blood, since the conditioned reduction of proliferation and cytokine production is completely abrogated after surgical denervation of the spleen. Thus, during conditioning, the CNS learns to reinstate at demand a CsA-like immunosuppression via splenic innervation. This might be used as a supportive therapy for controlling immune functions.

Animals↗
PubMed2006

The immune system and happiness.

Human ability to experience negative and positive emotions has an evolutionary perspective and the presence of feelings designed to influence behavior should thus be reflected in physiological and immune interactions. The complex interactions between the immune system and the central nervous system have been studied extensively in schizophrenia and depression. On the other hand, effects of positive human emotions, especially happiness, on physiological parameters and immunity have received very little attention. Emotions are intimately involved in the initiation or progression of cancer, HIV, cardiovascular disease, and autoimmune disorders. The specific physiological responses induced by pleasant stimuli were recently investigated with the immune and endocrine systems being monitored when pleasant stimuli such as odors and emotional pictures were presented to subjects. The results revealed that an increase in secretory immunoglobulin A and a decrease in salivary cortisol were induced by pleasant emotions. The mechanisms by which positive as opposed to negative states are instantiated in the brain and interact with the immune system are not yet understood. The present review investigates relations among physiological measures of affective style, psychological well-being, and immune function. There is data to support the hypothesis that individuals characterized by a more negative affective style poorly recruit their immune response and may be at risk for illness more so than those with a positive affective style. Future research is needed to expand our knowledge of the physiological and immune interactions of positive emotional states and their beneficial effects on health.

Brain↗
PubMed1999

Surgery, pain, and immune function.

Research findings have demonstrated that surgery negatively affects immune function. Pain also has deleterious effects on immune function. Most research in this area has been conducted on animals. Psychoneuroimmunology provides the framework for this article. Psychoneurological phenomena, such as stress, depression, and pain, can influence immune system functioning through neuroendocrine pathways. Biological and behavioral processes appear to be closely related and need to be jointly considered when planning and providing anesthesia care. The anesthesia planning process increasingly involves aggressive assessment and treatment of postoperative pain, which may benefit immune function.

Anesthesia↗